While NDUFAF6 is implicated in breast cancer, its specific role remains unclear.

The expression levels and prognostic significance of NDUFAF6 in breast cancer were assessed using The Cancer Genome Atlas, Gene Expression Omnibus, Kaplan-Meier plotter and cBio-Portal databases. We knocked down NDUFAF6 in breast cancer cells using small interfering RNA and investigated its effects on cell proliferation and migration ability. We performed gene expression analysis and validated key findings using protein analysis. We also assessed mitochondrial activity and cellular metabolism.

NDUFAF6 was highly expressed in breast cancer, which was associated with a poorer prognosis. Knockdown of NDUFAF6 reduced the proliferation and migration ability of breast cancer cells. Transcriptome analysis revealed 2,101 differentially expressed genes enriched in apoptosis and mitochondrial signaling pathways. Western blot results showed NDUFAF6 knockdown enhanced apoptosis. In addition, differential gene enrichment analysis was related to mitochondrial signaling pathways, and western blot results verified that mitophagy was enhanced in NDUFAF6 knockdown breast cancer cells. JC-1 assay also showed that mitochondrial dysfunction and reactive oxygen species content were increased after knocking down NDUFAF6. In addition, basal and maximal mitochondrial oxygen consumption decreased, and intracellular glycogen content increased.

Knockdown of NDUFAF6 resulted in apoptosis and mitophagy in breast cancer cells and NDUFAF6 may be a potential molecular target for breast cancer therapy.

mtDNA mutator mice (Polgmut/mut mice) have reinforced the mitochondrial theory of aging. These mice accumulate multiple mutations in mtDNA with age due to a homozygous proofreading-deficient mutation in mtDNA polymerase gamma (Polg), resulting in mitochondrial respiratory dysfunction and premature aging phenotypes. However, whether the accumulation of multiple mutations in Polgmut/mut mice induces mitochondrial respiratory dysfunction remains unclear. Here, we determined the accurate mtDNA genotype, including the frequency of total mutations and the number of non-synonymous substitutions and pathogenic mutations, using next-generation sequencing in the progeny of all three genotypes obtained from the mating of heterozygous mtDNA mutator mice (Polg+/mut mice) and examined their correlation with mitochondrial respiratory activity. Although Polg+/mut mice showed equivalent mtDNA genotype to Polg+/+ (wild-type) mice, the mitochondrial respiratory activity in the Polg+/mut mice was mildly reduced. To further investigate the causal relationship between mtDNA genotype and mitochondrial respiratory activity, we experimentally varied the mtDNA genotype in Polg mice. However, mitochondrial respiratory activity was mildly reduced in Polg+/mut mice and severely reduced in Polgmut/mut mice, regardless of the mtDNA genotype. Moreover, by varying the mtDNA genotype, some Polg+/+ mice showed mtDNA genotype equivalent to those of Polgmut/mut mice, but mitochondrial respiratory activity in Polg+/+ mice was normal. These results indicate that the mitochondrial respiratory dysfunction observed in mice with proofreading-deficient mutation in Polg is correlated with the nuclear genotype of Polg rather than the mtDNA genotype. Thus, the mitochondrial theory of aging in Polgmut/mut mice needs further re-examination.

Antioxidants had a growing interest owing to their protective roles in food and pharmaceutical products against oxidative deterioration and in the body and against oxidative stress-mediated pathological processes. Screening of antioxidant properties of plants and plant derived compounds requires appropriate methods, which address the mechanism of antioxidant activity and focus on the kinetics of the reactions including the antioxidants. Many studies have been conducted with evaluating antioxidant activity of various samples of research interest using by different methods in food and human health. These methods were classified methods described and discussed in this review. Methods based on inhibited autoxidation are the most suited for termination-enhancing antioxidants and, for chain-breaking antioxidants while different specific studies are needed for preventive antioxidants. For this purpose, the most commonly methods used in vitro determination of antioxidant capacity of food and pharmaceutical constituents are examined and also a selection of chemical testing methods is critically reviewed and highlighting. In addition, their advantages, disadvantages, limitations and usefulness were discussed and investigated for pure molecules and raw plant extracts. The effect and influence of the reaction medium on performance of antioxidants is also addressed. Hence, this overview provides a basis and rationale for developing standardized antioxidant capacity methods for the food, nutraceuticals, and dietary supplement industries. Also, the most important advantages and shortcomings of each method were detected and highlighted. The underlying chemical principles of these methods have been explained and thoroughly analyzed. The chemical principles of methods of 1,1-diphenyl-2-picrylhydrazyl (DPPH•) radical scavenging, 2,2'-azinobis-(3-ethylbenzothiazoline-6-sulphonate) radical (ABTS·+) scavenging, ferric ions (Fe3+) reducing assay, ferric reducing antioxidant power (FRAP) assay, cupric ions (Cu2+) reducing power assay (Cuprac), Folin-Ciocalteu reducing capacity (FCR assay), superoxide radical anion (O2·-), hydroxyl radical (OH·) scavenging, peroxyl radical (ROO·) removing, hydrogen peroxide (H2O2) decomposing, singlet oxygen (1O2) quenching assay, nitric oxide radical (NO·) scavenging assay and chemiluminescence assay are overviewed and critically discussed. Also, the general antioxidant aspects of the main food and pharmaceutical components were discussed through several methods currently used for detecting antioxidant properties of these components. This review consists of two main sections. The first section is devoted to the main components in food and their pharmaceutical applications. The second general section includes definitions of the main antioxidant methods commonly used for determining the antioxidant activity of components. In addition, some chemical, mechanistic, and kinetic properties, as well as technical details of the above mentioned methods, are provided. The general antioxidant aspects of main food components have been discussed through various methods currently used to detect the antioxidant properties of these components.

The role of reactive oxygen species (ROS) in cellular senescence and inflammation has been extensively studied; however, the specific molecular mechanisms underlying these effects have yet to be fully elucidated. By applying a nucleotide pool detection system, oxidative microRNA sequencing, and cytokine chip detection techniques, we found that the levels of 8-oxo-guanosine triphosphate (8-oxo-GTP) increased with age and were positively correlated with elevated levels of oxidized microRNA and increased levels of inflammatory factors. During aging, guanine residues in the seed regions of miR-98-5p that regulates ICAM1, and miR-8085 that regulates CXCL16, were oxidized to 8-oxoguanine. This oxidation weakened the binding affinity of microRNAs to their target genes, thereby promoting the expression of ICAM1 and CXCL16. Oxidized microRNAs can regulate new target genes via o8G:A base mismatches. Our findings reveal that ROS-induced oxidative modifications of microRNAs reshape gene regulatory networks, activate inflammatory pathways, providing new insights into the mechanisms of age-related inflammation.

We focused on evaluating oxidative stress as a major mechanism of cell damage in patients with COVID-19 infection by simultaneously assessing standard oxidative stress biomarkers in vivo-for the very first time in this specific combination-alongside typical clinical biomarkers of inflammation. Standard biomarkers were used to evaluate the oxidative stress status and antioxidant activity in the blood plasma of COVID-19 patients and healthy controls. These included TBARSs (Thiobarbituric Acid-Reactive Substances), SOD (Super Oxide Dismutase), CAT (catalase), GRA (glutathione reductase) activities, and AOC (antioxidant capacity). All clinical inflammation data confirmed a highly activated immune response in the tested COVID-19 patients: WBCs (white blood cells) were increased by nearly 100%, LYMs (lymphocytes) increased by ~30%, CRP (C-reactive protein) rose by over 2200%, and the ESR (erythrocyte sedimentation rate) increased by ~320% compared to established maximum control levels. The results confirmed that the infection involved a free-radical-mediated damage mechanism: TBARS levels increased almost 3-fold, the AOC decreased more than 4-fold, SOD was increased nearly 5-fold, CAT was increased by 1.4 times, and GRA was suppressed by 2.5 times. COVID-19 was associated with oxidative stress and suppressed antioxidant activity. All these changes contribute to the severity of the disease, complications, and mortality in COVID-19 patients.

This study evaluated the antioxidant capacity of the oxidation products of three flavonols using oxygen radical absorbance capacity-fluorescein assay (ORAC-FL), oxygen radical absorbance capacity-pyrogallol red assay (ORAC-PGR), and the cellular antioxidant activity (CAA) assay in human dermal fibroblast (HFF) cells, with 2,2'-azobis(2-amidinopropane) dihydrochloride (AAPH) as a free radical generator under controlled pH and solvent conditions. At pH 2 in a polar aprotic solvent, BZF-OH (benzofuranone-OH) compounds were formed, while methoxylated analogs were obtained at pH 7 in a polar protic solvent. The products generated at pH 2 exhibited significantly higher antioxidant capacities, demonstrating the influence of the reaction environment on modulating antioxidant properties. The antioxidant activity was observed to reflect the combined action of the flavonol precursor and its oxidation products. This led to the proposal of the Gross Antioxidant Capacity (GAC) concept to integrate the contribution of all generated species. Since chemical assays such as ORAC do not fully capture the complexity of biological systems, they should be complemented with cellular approaches for a more accurate evaluation. Additionally, BZF-OH compounds were analyzed as potential cyclooxygenase-2 (COX-2) inhibitors through docking and molecular dynamics simulations, where BZF-Quer-OH showed binding affinities comparable to celecoxib, a selective COX-2 inhibitor. These findings were complemented by an analysis of COX-2 expression in RAW 264.7 cells treated with lipopolysaccharide (LPS), where treatment with the antioxidants significantly inhibited COX-2 expression. In the case of the oxidation products, only the oxidation product of rhamnetin showed a reduction in COX-2 expression compared to the LPS-treated control. Together, these results highlight that flavonol-derived oxidation products not only retain significant antioxidant capacity but may also possess anti-inflammatory properties, opening new perspectives for the development of innovative therapies targeting oxidative stress and chronic inflammation.

Amyloid-beta (Aβ) aggregates, an Alzheimer's disease (AD) pathological hallmark, extend beyond the brain to the heart of heart failure (HF) and AD patients. Being diseases of the elderly, increased prevalence is expected as the population ages. However, changes in the incidence and prevalence of dementia over the past decades, and the independent association of exposure to air particulate matter (PM) with poor cognitive function, adverse cardiovascular effects, and oxidative stress hint to the contribution of other factors beyond senescence. Therefore we evaluate whether, and by which mechanism(s), PM exposure affects heart and brain proteinopathy with/without genetic predisposition.AD-prone and control mice are exposed for three months to filtered air (FA) or concentrated ambient PM < 2.5μm in diameter (PM2.5), and evaluated for Aβ pathology, cognitive and cardiac function, and markers of oxidative stress. Aβ pathology become noticeable in AD hearts and worsens with PM2.5 in AD brains. Functionally, PM2.5 lead to anxiety and memory deficits and worsens diastolic function. Redox homeostasis is negatively impacted by genotype and PM2.5. This study identifies environmental pollution as a potential key contributor to early progression of heart and brain proteinopathy, delineating a crucial timepoint for early interventions to limit multiorgan damage in vulnerable patients.

Animal proteins are the primary global protein source, but their production is environmentally challenging and has low conversion efficiency. This highlights the need to diversify dietary protein sources. Algal proteins provide a sustainable alternative, outperforming traditional plant and animal proteins in protein content, quality, and digestibility. Furthermore, bioactive peptides (BAPs) derived from algal proteins exhibit significant health benefits, including antihypertensive, antioxidant, antimicrobial, anticancer, and antidiabetic activities. This review comprehensively explores the nutritional benefits of algal proteins and provides an innovative summary of the production techniques for algal bioactive peptides. It also highlights the synergistic application methods of these technologies. By integrating pretreatment methods such as ultrasound-assisted extraction, pulsed electric field, and high hydrostatic pressure with enzymatic-assisted extraction, these techniques demonstrate a synergistic effect in improving protein hydrolysis efficiency while also increasing the yield of BAPs. Meanwhile, database resources related to algal proteins are integrated and the application of computer technology in the development of algal proteins is analyzed. It aims to provide new insights to optimize the development and utilization of algal proteins to help them become a sustainable source of nutrition to meet the needs of a growing global population.

With an increasing focus on healthier dietary alternatives, this study developed a protein-rich, ready-to-cook flatbread premix using millet, pulse, and oilseed flours. The premix offers a balanced nutritional profile, providing high protein content (∼21%) and delivering 423 kcal/100 g. It demonstrated phenolic content of 0.98 mg catechin equivalents/gram of premix, which increased to 1.90 mg catechin equivalents/gram of cooked (lyophilized) product. Antioxidant activity was evaluated through DPPH radical scavenging, yielding values of 5.28 nmol Trolox equivalents per gram for the premix and 4.82 nmol Trolox equivalents per gram for the cooked product. Similarly, hydroxyl radical scavenging activity was measured at 4.38 µmol Trolox equivalents per gram for the premix and 4.36 µmol Trolox equivalents per gram for the cooked product. The product was highly acceptable in sensory evaluations, indicating strong potential for consumer adoption. In vivo studies with Balb/c mice revealed no adverse effects on oxidative stress levels or immune function. The flatbread promoted a healthy gut microbiota composition, supporting gut health while maintaining cellular oxidative balance. Hematological analyses showed improved white blood cell and lymphocyte counts, reflecting enhanced immune resilience. These findings highlight the premix as a promising dietary alternative to traditional carbohydrate-rich staples. With its nutrient density and functional benefits, the flatbread premix offers a practical solution for improving dietary habits and addressing lifestyle-related health concerns. This study underscores the importance of incorporating such functional foods into daily diets to promote better health and prevent nutrition-related disorders. Further research is warranted to explore its broader health impacts over extended durations. PRACTICAL APPLICATION: The ready-to-cook flatbread premix made from millets, pulses, and oilseeds offers a simple and nutritious way to enhance daily diets. Rich in protein and supplemented with various oilseeds as a source of polyunsaturated fatty acids, it provides a healthier alternative to regular flatbreads. It is convenient and ideal for maintaining a balanced diet and also supports the management of lifestyle-related health issues such as obesity. With its antioxidant properties and ability to support a healthy gut microbiota, this flatbread contributes to overall health. It promotes better eating habits without compromising taste or convenience.

The oxidation of an aromatic ring in guanosine monophosphate by a RuII-aqua complex, [RuII(OH2)(η5-C5Me5)(bpy)]+ (bpy = 2,2'-bipyridine), using O2 gases in an aqueous solution has been reported (Takenaka et al. Chem. Asian J. 2018, 13, 3480-3184). However, its mechanism has not been sufficiently clarified to facilitate the design of optimal catalysts. To clarify the mechanism of aerobic oxidation catalyzed by Ru complexes, we employed density functional theory (DFT) calculations to analyze the oxidation of 9-methyl guanine, as a model of the substrate. Although the ligand-exchange reaction between the H2O and O2 molecules yielded a more stable RuIV-peroxo complex, [RuIV(η2-O2)(η5-C5Me5)(bpy)]+, subsequent reactions were initiated by a RuIII-superoxo complex, [RuIII(η1-O2•-)(η5-C5Me5)(bpy)]+. We confirmed the plausible path for the homolytic cleavage of the O-O bond in [RuIII(η1-O2•-)(η5-C5Me5)(bpy)]+ to form a RuIV-oxo complex, [RuIV(O)(η5-C5Me5)(bpy)]+, with the activation free energy (ΔGa) of 12.2 kcal/mol. The subsequent oxidation of the substrate by [RuIV(O)(η5-C5Me5)(bpy)]+ facilitated the formation of an arenium-like intermediate to form the product compounds, where the energy in the transition state corresponding to the oxidation of the substrate is 21.5 kcal/mol. An additional reaction path for the oxidation of the substrate by [RuIII(η1-O2•-)(η5-C5Me5)(bpy)]+ must exceed the high energy in the transition state (31.7 kcal/mol), indicating that [RuIV(O)(η5-C5Me5)(bpy)]+ catalyzed the oxidation of the substrate as reactive species. Conversely, the Cp*-ligand oxidation, which induced catalyst degradation, requires ΔGa of 21.4 kcal/mol to exceed the transition state. Overall, our DFT study offers insight into the reaction mechanism of aerobic oxidation involving inert chemical bonds, facilitating the design of appropriate catalysts for the reaction.

8-Oxo-7,8-dihydroguanine (GO, 8-hydroxyguanine), an oxidatively damaged base, induces mutations and is involved in cancer initiation. In addition to G:C→T:A transversions at the damaged site, it causes untargeted base substitution (action-at-a-distance) mutations at the G bases of 5'-GpA-3' sites in human cells. Paradoxically, OGG1, a DNA glycosylase involved in the base excision repair (BER) pathway, enhances the action-at-a-distance mutations by GO. In this study, other DNA glycosylases, potential repair enzymes for the GO base, were knocked down, and their effects on the untargeted mutations were examined using the supF reporter gene. The knockdown of NEIL1 decreased such mutations, while those of NTH1, NEIL2, and NEIL3 had no effects. The double knockdown of OGG1 and NEIL1 additively affected the mutation frequency. These results indicated that NEIL1 is another BER protein involved in the action-at-a-distance mutations triggered by the oxidized guanine base.

The relationship between dietary vitamin E intake and the risk of cardiovascular diseases, as well as cardiovascular and all-cause mortality, remains inconclusive. This study aimed to investigate these associations in a large, representative sample of the U.S. population.

We analyzed data from 39,293 participants in the National Health and Nutrition Examination Survey (NHANES) 2003-2018. Dietary vitamin E intake was assessed using 24-h recall data. Outcomes included incident cardiovascular disease (CVD), CVD mortality, and all-cause mortality. We employed weighted logistic and Cox regression models, adjusting for potential confounders. Restricted cubic spline (RCS) analyses and were conducted to assess non-linear relationships.

Compared to participants with a vitamin E intake of 4.08 mg or lower (lowest quartile), the multivariable-adjusted odds ratio for those with an intake of 9.86 mg or higher (highest quartile) was 0.57 (95 % CI, 0.50-0.64) for cardiovascular disease (P for trend <0.01). The multivariable-adjusted hazard ratios for participants with a vitamin E intake of 9.86 mg or higher were 0.85 (95 % CI, 0.75-0.98) for all-cause mortality (P for trend = 0.04) and 0.96 (95 % CI, 0.76-1.21) for CVD mortality (P for trend <0.001). RCS analyses revealed non-linear associations for most outcomes, including overall CVD, coronary heart disease, heart attack, stroke, and all-cause mortality (all P-nonlinear <0.05).

In this large NHANES cohort, higher dietary intake of vitamin E was associated with reduced risks of cardiovascular disease and all-cause mortality. These findings suggest potential benefits of vitamin E-rich diets in cardiovascular health promotion and mortality reduction.

Aging and age-related neurodegenerative disorders are characterized by the dysfunction or loss of brain nicotinic acetylcholine receptors (nAChRs), and these changes may be related to other senescence markers, such as oxidative stress and DNA repair dysfunction. However, the mechanism of nAChR loss in the aging brain and the modification of this process by drugs (e.g., memantine, Mem) are not yet fully understood. To study whether the differences in nAChR expression in the rat brain occur due to aging or oxidative stress and are modulated by Mem, we analyzed nAChR subunits (at RNA and protein levels) and other biomarkers by real-time quantitative polymerase chain reaction (RQ-PCR) and Western blot validation. Twenty-one female Wistar rats were divided into four groups, depending on age, and the oldest group received injections of Mem or water with the use of intragastric catheters. We studied the cerebral grey matter (CGM), subcortical white matter (SCWM), and cerebellum (Ce). Results showed an age-related decrease of α7 nAChR mRNA level in SCWM. The α7 nAChR mRNA loss was accompanied by reduced expression of 8-oxoguanine DNA glycosylase 1 (OGG1) and an increased tumor necrosis factor alpha (TNFα) level. In the water group, we observed a higher level of α7 nAChR protein in the SCWM and Ce. Biomarker levels changed, but to a different extent depending on the brain area. Importantly, the dysfunction in antioxidative status was stopped and even regressed under Mem treatment. After two weeks of treatment, an increase in TP53 protein level and a decrease in 8-oxo-2'deoxyguanosine (8-oxo-2'dG) level were observed. We conclude that Mem administration may be protective against the senescence process by antioxidative mechanisms.

Eggplant is a nutritionally rich crop that has beneficial effects on human health. Wide diversity exists in eggplant in terms of biochemical content; however, extensive research work has not been undertaken to gain more in-depth knowledge on its antioxidant capacity to improve the quality of the existing popular cultivated varieties and develop/identify nutrient-rich germplasms. Therefore, a total of 57 genotypes were chosen for the study, and they were evaluated for various biochemical compounds. The biochemical traits taken were an average of three replications and these values were used for statistical analysis. The analysis of variance for five fruit quality parameters indicated a high variability among the eggplant genotypes, which signifies that at least one of the genotypes is statistically different from the rest. The total phenolics ranged from 39.63 to 312.65 mg gallic acid equivalent (GAE)/100 g with the highest being observed in Pusa Krishna. The flavonoid content ranged from 7.83 to 65.09 mg/100 g FW. The antioxidant assays, viz., cupric reducing antioxidant activity (CUPRAC) and ferric reducing antioxidant power (FRAP), were evaluated which ranged from 51.48 to 200.36 mg GAE/100 g for CUPRAC and 35.36 to 214.01 mg GAE/100 g for FRAP. Principal component analysis (PCA) generated a total of five principal components, and the maximum variance of 90.72% was exhibited by the first three PCs. The agglomerative hierarchical clustering (AHC) revealed similar results to the PCA by identifying three major clusters. Cluster 1 had a maximum number of genotypes grouped together, i.e., 48, followed by cluster 2 with six genotypes, viz., Pusa Krishna (G-32), G-5, Mayurbhanj Local, HABI-2, Solanum gilo, and Solanum sisymbrifolium, and cluster 3 had only three genotypes, namely, Solanum insanum, Solanum khasianum, and Solanum xanthocarpum. Furthermore, the wild species S. insanum, S. khasianum, and S. xanthocarpum can also be utilized as a donor line for carrying out the nutritional breeding program as they are the reservoir of many important biochemical genes.

In recent years, there have been significant advances in pathological research on alcoholic liver disease (ALD), with suitable animal models making a significant contribution. However, the currently established animal ALD models still have some significant drawbacks, especially the inability to induce the entire human ALD lineage, which may be related to physiological differences between animals and humans. This review comprehensively summarized the most widely used experimental models of ALD, including voluntary drinking, Lieber-DeCarli, Meadows-Cook, Tsukamoto-French, NIAAA, and the "second hit" model. "Second hit" refers to an additional factor that damages the liver. There are various "second hit" models that fall into two main categories: particular diets and drugs. These models can either simulate human drinking patterns more accurately or produce varying degrees of ALD without significantly increasing animal mortality. We introduced the established method of the original models, discussed the advantages and disadvantages of the existing models from the aspects of operability and practicality, and provided existing improvement methods, hoping to provide a reference for future researchers.

Mitochondria are vital organelles found within living cells and have signalling, biosynthetic, and bioenergetic functions. Mitochondria play a crucial role in metabolic reprogramming, which is a characteristic of cancer cells and allows them to ensure a steady supply of proteins, nucleotides, and lipids to enable rapid proliferation and development. Their dysregulated activities have been associated with the growth and metastasis of different kinds of human cancer, particularly ovarian carcinoma. In this review, we briefly demonstrated the modified mitochondrial function in cancer, including mutations in mitochondrial DNA (mtDNA), reactive oxygen species (ROS) production, dynamics, apoptosis of cells, autophagy, and calcium excess to maintain cancer genesis, progression, and metastasis. Furthermore, the mitochondrial dysfunction pathway for some genomic, proteomic, and metabolomics modifications in ovarian cancer has been studied. Additionally, ovarian cancer has been linked to targeted therapies and biomarkers found through various alteration processes underlying mitochondrial dysfunction, notably targeting (ROS), metabolites, rewind metabolic pathways, and chemo-resistant ovarian carcinoma cells.

Late-onset hypogonadism (LOH) is a common age-related condition in men, characterized by a decline in serum testosterone and a range of associated signs and symptoms, and is classified as impotence in traditional medicine. Saffron is the dried stigma of Crocus sativus L., which is used in traditional medicine as an aphrodisiac.

This study aimed to investigate the effects of saffron extract (SE) on LOH using an aging mouse model and Leydig cells.

The potential mechanisms and therapeutic targets of SE for the treatment of LOH were first identified using network pharmacology. An aging model was induced in mice by administration of D-galactose, followed by treatment with varying concentrations of SE. Subsequent assessments of serum testosterone levels, semen quality, testicular aging, oxidative stress, and apoptotic markers were performed to assess the impact of SE and to elucidate its mechanisms. In addition, in vitro experiments assessed the effect of SE on Leydig cell viability, oxidative stress, and apoptosis.

The results showed that SE could modulate the PI3K-Akt-Nrf2 signaling pathway, enhancing Leydig cell resistance to oxidative stress and reducing Leydig cell apoptosis, thereby improving Leydig cell function and alleviating the decrease in serum testosterone associated with aging.

Saffron is a promising strategy for the treatment of LOH and provides an effective approach to alleviate serum testosterone decline in older men.

Licochalcone A (LicoA) possesses anti-tumor properties. However, the potential therapeutic effect of LicoA on uterine leiomyomas (ULs) remains unknown. In this study, the effects of LicoA on the proliferation of ULs and its underlying mechanism were explored. LicoA treatment significantly decreased the viability of uterine smooth muscle cells (UtSMCs) and ELT3 cells in a dose-dependent manner. The induction of ELT3 cell apoptosis by LicoA was accompanied by the increased generation of reactive oxygen species (ROS), elevated endoplasmic reticulum (ER) stress (GRP78/IRE1α/ATF6/CHOP), and the increased expression of proapoptotic proteins (c-caspase-3, c-caspase-9, and c-PARP). The ability of Z-VAD-FMK (a caspase inhibitor) and n-acetylcysteine (NAC; a cell membrane permeable antioxidant) to reverse LicoA-induced ROS-mediated ER stress pathways also observed. Furthermore, GRP78 or JNK knockdown was involved in LicoA-induced ROS-mediated ER stress and apoptosis in ELT3 cells. In immunodeficient mice, LicoA significantly suppressed the growth of ELT3 tumor cells, without toxicity. This study is the first to show that LicoA exerts anti-leiomyoma effects via the modulation of ROS-mediated ER stress-induced apoptosis through the JNK/GRP78/NRF2 signaling pathway.

1,4-dihydropyrimidine-2-thiones were synthesized in five series that include 5-carboxylic acid derivatives of dihydropyrimidine (series A, 6-8), novel 5-carboxamide derivatives of dihydropyrimidine (series B, 9-14), N,S-dimethyl-dihydropyrimidine (series C, 15-20), N-hydrazinyl derivatives of dihydropyrimidine (series D, 21-24) and tetrazolo dihydropyrimidine derivatives (series E, 25-28), and evaluated for anti-diabetic capability. The prepared novel compounds were structurally established by FTIR, 1HNMR, 13CNMR, ESI and HRMS. All of these compounds from series A-E were first time examined for α-glucosidase inhibition as to evaluate their anti-diabetic potential. Most of the compounds for example 8, 11-14, 15, 17-21, 25 and 28 demonstrated greater α-glucosidase inhibitory effects (IC50 = 12.5 ± 0.21 to 47.3 ± 0.23 μM) when compared to deoxynojirimycin as standard (IC50 = 52.02 ± 0.36 μM). Compounds from series B and C found to be highly active however, the compounds from series D found generally less active. The structure-activity relationships demonstrated the importance of C-5 carboxamides, C-5 ethyl ester functionality, and the presence of N,S-dimethyl groups at pyrimidine ring for α-glucosidase inhibition. The docking studies demonstrated that all the active compounds have van der Waals and alkyl bonds interactions with the targeted site of the human lysosomal acid α-glucosidase. All these compounds were also tested for antioxidant potential by DPPH radical scavenging protocol that exhibited significant antioxidant effects (IC50 = 21.4 ± 0.45 to 92.1 ± 0.38 μM) as compared to the standard butylated hydroxyanisol (IC50 = 44.2 ± 0.36 μM). Among all, compound 13, 14 and 19 with potent α-glucosidase inhibition (IC50 = 18.9 ± 0.72, 23.3 ± 0.45 and 21.5 ± 0.16 µM, respectively) along with excellent antioxidant potential in the range of (IC50 = 21.4 ± 0.45 to 31.2 ± 0.23 μM) indicated their ability to use as valuable leads for the development of anti-diabetic drugs with the combined effects of antioxidants.

Maejo 341 Sweet potato (MSP) is a new purple sweet potato variety cultivated in Northern Thailand, but its health benefits are unknown. This study aimed to investigate its antioxidant, anti-inflammatory, and anti-osteoporotic activities, as well as its anthocyanin content. The peel and flesh of MSP were extracted with ethanol and water. Compared with the flesh extracts, the peel extracts presented greater antioxidant capacity and were rich in phenolics, flavonoids, and anthocyanins, namely, cyanidin-3-O-glucoside, peonidin-3-O-glucoside, pelargonidin-3-O-glucoside, cyanidin, and peonidin. The peel extracts suppressed lipopolysaccharide-induced inflammation by inhibiting the secretion of proinflammatory cytokines and enzymes, including TNF-α, IL-1β, IL-6, COX-2, and iNOS, as well as reducing nitric oxide and matrix metalloproteinase-9 secretion. The extracts inhibited the RANKL-induced NF-κB and MAPK pathways and downregulated osteoclastogenic marker expression. Under LPS and RANKL treatment, the peel extracts notably reduced reactive oxygen species production while increasing antioxidant gene expression. Furthermore, they increased osteoblast viability and slightly raise alkaline phosphatase activity. These findings suggest that MSP peel could be used as a functional food to alleviate oxidative stress and inflammation-related osteoporosis.

ROS cause multiple forms of DNA damage, and among them, 8-oxoguanine (8-oxoGua), an oxidized product of guanine, is one of the most abundant. If left unrepaired, 8-oxoGua may pair with A instead of C, leading to a mutation of G: C to T: A during DNA replication. 8-Oxoguanine DNA glycosylase 1 (OGG1) is a tailored repair enzyme that recognizes 8-oxoGua in DNA duplex and initiates the base excision repair (BER) pathway to remove the lesion and ensure the fidelity of the genome. The accumulation of genomic 8-oxoGua and the dysfunction of OGG1 is readily linked to mutagenesis, and subsequently aging-related diseases and tumorigenesis; however, the direct experimental evidence has long been lacking. Recently, a series of studies have shown that guanine oxidation in the genome has a conservative bias, with the tendency to occur in the regulatory regions, thus, 8-oxoGua is not only a lesion to be repaired, but also an epigenetic modification. In this regard, OGG1 is a specific reader of this base modification. Substrate recognition and/or excision by OGG1 can cause DNA conformation changes, affect chromatin modifications, thereby modulating the transcription of genes involved in a variety of cellular processes, including inflammation, cell proliferation, differentiation, and apoptosis. Thus, in addition to the potential mutagenicity, 8-oxoGua may contribute to tumor development and progression through the altered gene expression stemming from its epigenetic effects.

In response to growing concerns about the health effects of quasi-millimeter waves (qMMW) used in 5th-generation wireless systems, conservative whole-body exposure thresholds based on indirect evidence have been proposed. The guidelines define a whole-body average specific absorption rate (WBA-SAR) of 4 W/kg which causes a 1 °C increase in core temperature, as the operational threshold for adverse health effects. To address the lack of direct evidence, we recently reported that a 30-minute exposure to qMMW at 4.6 W/kg resulted in a 1 °C increase in rat core temperature. Here, we further analyzed the near-threshold stress response for the first time, using biological samples from the aforementioned and additional experiments.

A total of 59 young Sprague-Dawley rats (240-322 g) were exposed to 28 GHz for 40 minutes at WBA-SARs of 0, 3.7, and 7.2 W/kg, under normal (22.5 °C, 45-55% humidity), and heat (32 °C, 70% humidity) conditions. Rats were restrained in acrylic holders for dose control. We repeatedly measured serum and urinary biomarkers of stress response, aggregated the data, and analyzed them using a single statistical mixed model to subtract the effects of sham exposure and between-subject variation.

Sham exposure induced stress responses, suggesting an effect of restraint. After the subtraction of the sham exposure effect, 28 GHz appeared to induce stress responses as evidenced by elevated serum-free corticosterone 1 or 3 days after the exposure, which was more evident in animals with a change in rectal temperature exceeding 1 °C. Urinary-free catecholamines demonstrated an inhibitory property of 28 GHz frequency exposure on the stress response as evidenced by noradrenaline on the day of exposure. Heat exposure enhanced this effect, suggesting a possible role of noradrenaline in heat dissipation by promoting cutaneous blood flow, a notion supported by the correlation between noradrenaline levels and tail surface temperature, a critical organ for heat dissipation.

This study is the first to demonstrate that qMMW whole-body exposure can alter the stress response as indicated by corticosterone and noradrenaline at near-threshold levels. Our findings may provide insight into the biological basis of the whole-body exposure thresholds in the international guidelines.

The relationship between vitamin intake and diabetes mellitus (DM) has attracted growing attention. Only few studies have linked vitamin B2 (VB2) and development of DM. In this study, we aimed to assess the association between VB2 intake and DM among U.S. adults.

We performed a cross-sectional analysis by using four waves of the National Health and Nutritional Examination Surveys (NHANES) data in 2013-2020. A total of 18,338 participants aged ≥18 years were included. VB2 intake was estimated by 24-h dietary recall on the first day. We used multiple logistic regression analysis to assess the association between VB2 intake and DM in men and women, separately.

VB2 intake was significantly associated with DM in women but not in men (P-interaction < 0.05). In women, the multivariable-adjusted odds ratio (OR) for the fourth compared with the first quartile of VB2 intake was 0.67 (95% CI: 0.48, 0.93, P-trend = 0.025). Each standard deviation increment of log-transformed VB2 intake was associated with 19% reduced odds of DM (P = 0.005). In contrast, no significant association between VB2 intake and DM was observed in men (P-trend > 0.05). An inverse dose-response relationship between VB2 intake and DM was observed in women, but not in men.

Increased VB2 intake was associated with lower odds of DM in women, but not men. Our study underscores the potential role of VB2 in the prevention of DM in women. Prospective studies from different populations are warranted to confirm our findings.

Frozen surimi sol incline to protein oxidation, but the quality control strategies based on oxidation remain limited. Hence, the antioxidant and cryoprotective effects of γ-polyglutamic acid (γ-PGA) on freeze-thawed salt-dissolved myofibrillar protein (MP) sol were investigated. Results showed that γ-PGA could effectively regulate protein oxidation of MP sol during freeze-thawing with lower carbonyl contents and less oxidative cross-linking. Meanwhile, γ-PGA primely maintained sol protein structures, showing reduction of 15.28% of salt soluble protein contents at γ-PGA addition of 0.04% under unoxidized condition. Additionally, compared to the control group without oxidation treatment, cooking loss of heat-induced gel with 0.04% γ-PGA decreased by 47.19%, while gel strength obviously increased by 57.22% respectively. Overall, moderate γ-PGA addition (0.04%) could inhibit protein oxidation of sol, further improving frozen stability of sol through hydrogen bonds and hydrophobic interaction, but excessive γ-PGA was adverse to sol quality due to severe cross-linking between γ-PGA and MP.

The nervous system is susceptible to DNA damage and DNA repair defects, and if DNA damage is not repaired, neuronal cells can die, causing neurodegenerative diseases in humans. The overall picture of what is known about DNA repair mechanisms in the nervous system is still unclear. The current challenge is to use the accumulated knowledge of basic science on DNA repair to improve the treatment of neurodegenerative disorders. In this review, we summarize the current understanding of the function of DNA damage repair, in particular, the base excision repair and double-strand break repair pathways as being the most important in nervous system cells. We summarize recent data on the proteins involved in DNA repair associated with neurodegenerative diseases, with particular emphasis on PARP1 and ND-associated proteins, which are involved in DNA repair and have the ability to undergo liquid-liquid phase separation.

The considerable changes in lifestyle patterns primarily affect the human gut microbiota and result in obesity, diabetes, dyslipidemia, renal complications, etc. though there are few traditional safeguards such as herbal brews to maintain the ecological stability under intestinal dysbiosis. The present article is designed to collect all the scientific facts in a place to decipher the role of the Indian traditional herbal brews used to balance gut health for centuries. Computerized databases, commercial search engines, research papers, articles, and books were used to search by using different keywords to select the most appropriate published articles from 2000 onward to September 2023. A total of 1907 articles were scrutinized, 46 articles were finally selected from the 254 screened, and targeted information was compiled. Interaction of herbal brews to the gut microflora and resulting metabolites act as prebiotics due to antimicrobial, anti-inflammatory, and antioxidant properties, and modulate the pH of the gut. The effect of brews on gut microbiota has a drastic impact on various gut-related diseases and has gained popularity as an alternative to antibiotics against bacteria, fungi, viruses, parasites, and boosting the immune system and strengthening the intestinal barrier. Berberine, kaempferol, piperine, and quercetin have been found in more than one brew discussed in the present article. Practically, these brews balance the gut microbiota, prevent chronic and degenerative diseases, and reduce organ inflammation, though, there is a knowledge gap on the molecular mechanism to explain their efficacy. Indian traditional herbal brews used to reboot and heal the gut microbiota since centuries-old practice with successful history without toxicity. The systematic consumption of these brews under specific dietary prescriptions has a hope of arrays for a healthy human gut microbiome in the present hasty lifestyle with overall health and well-being.

Parkinson's disease (PD) is a common neurodegenerative disease in the older adults. The main pathological change in PD is the degenerative death of dopamine (DA) neurons in the midbrain substantia nigra, which causes a significant decrease in the DA content of the striatum. However, the exact etiology of this pathological change remains unclear. Genetic factors, environmental factors, aging, and oxidative stress may be involved in the degenerative death of dopaminergic neurons in PD. Pharmacological treatment using levodopa (L-DOPA) remains the main treatment for PD. Most patients with PD consuming L-DOPA for a long time usually develop levodopa-induced dyskinesia (LID) after 6.5 years of use, and LID seriously affects the quality of life and increases the risk of disability. Recently, studies have revealed that cerebral iron deposition may be involved in LID development and that iron deposition has neurotoxic effects and accelerates disease onset. However, the relationship between cerebral iron deposition and LID remains unclear. Herein, we reviewed the mechanisms by which iron deposition may be associated with LID development, which are mainly related to oxidative stress, neuroinflammation, and mitochondrial and lysosomal dysfunction. Using iron as an important target, the search and development of safe and effective brain iron scavengers, and thus the alleviation and treatment of LID, has a very important scientific and clinical value, as well as a good application prospect.

Diphenylamine (DPL) has been widely utilized in industrial chemicals, but its degradation by HO• radicals in the environment has not been fully studied yet. The present study uses quantum chemical calculations to evaluate the reaction of DPL with HO• radicals in atmospheric and aqueous environments. The results showed that, in the atmosphere, the diphenylamine reacted with the HO• radical rapidly, with an overall rate constant of 9.24 × 1011 to 1.34 × 1011 M-1 s-1 and a lifetime of 0.17 to 1.55 h at 253-323 K. The calculated overall rate constant in water (koverall = 1.95 × 1010 M-1 s-1, pH = 3-14) is in excellent agreement with the experimental value (koverall = 1.00 × 1010-1.36 × 1010 M-1 s-1). The HO• + DPL reaction in water could occur following the hydrogen transfer (15.4%), single electron transfer (41.6%), and radical adduct formation (41.7%) mechanisms, clarifying that addition products were not exclusive products. Nevertheless, variations in temperature and pH within aqueous environments had an impact on the mechanisms, kinetics, and degradation products of the reaction of DPL with HO• radicals.

A bioassay-guided isolation on the plant Zanthoxylum armatum DC yielded compounds tambulin (1), and prudomestin (2), from ethyl acetate fraction which showed the highest ROS inhibiting activity (IC50 = 17.8 ± 1.1 µg/mL). Structure elucidation of pure compounds was done using mass and NMR spectroscopic techniques. Compounds 1 and 2 revealed potent ROS inhibition with IC50 = 7.5 ± 0.3 and 1.5 ± 0.3 µg/mL, respectively, as compared to standard ibuprofen (IC50 = 11.2 ± 1.9 µg/mL). Likewise, both compounds 1 and 2 showed potent antioxidant activity with IC50 = 32.65 ± 0.31 and 26.96 ± 0.19 µg/mL, respectively. In vitro studies were supported by molecular docking and drug-likeliness properties. In silico studies of 1 and 2 with cyclooxygenase-2 (COX-2) showed perfect binding affinity with binding energies of -8.4 and -8.6 kcal/mol, respectively, comparable to standard ibuprofen (-7.7 kcal/mol). Drug likeness and ADMET showed higher gastrointestinal absorption of 1 and 2 and no toxic impact.

Our skin serves as the primary barrier against external environmental insults, the latter of which can cause oxidative stress within cells, while various bioactive peptides sourced from natural resources hold promise in protecting cells against such oxidative stress. In this study, we investigate the efficacy of a low molecular weight extract from the sea cucumber Apostichopus japonicus, denoted as Sample-P, in facilitating cell migration and wound healing under oxidative stress conditions in skin cells. The naturally derived compound is a highly complex mix of peptides exhibiting antioxidative properties, as highlighted through liquid chromatography-mass spectrometry peptide screening and an in vitro antioxidant assay. Our results demonstrate that Sample-P is capable of promoting cell migration while preventing severe stress responses such as visible through mTOR expression. To further identify the molecular pathways underpinning the overall protective mechanism of Sample-P, we have utilised a proteomics approach. Our data reveal that Sample-P regulates protein expression associated with ribosomal pathways, glycolysis/gluconeogenesis and protein processing in the endoplasmic reticulum (ER), which help in preserving DNA integrity and safeguarding cellular organelles, such as mitochondria and the ER, under oxidative stress conditions in skin cells. In summary, in the presence of H2O2, Sample-P exhibits antioxidative properties at both molecular and cellular levels, rendering it a promising candidate for topical skin treatment to wound healing and to address age-related skin conditions.

The genome duplication program is affected by multiple factors in vivo, including developmental cues, genotoxic stress, and aging. Here, we monitored DNA replication initiation dynamics in regenerating livers of young and old mice after partial hepatectomy to investigate the impact of aging. In young mice, the origin firing sites were well defined; the majority were located 10-50 kb upstream or downstream of expressed genes, and their position on the genome was conserved in human cells. Old mice displayed the same replication initiation sites, but origin firing was inefficient and accompanied by a replication stress response. Inhibitors of the ATR checkpoint kinase fully restored origin firing efficiency in the old mice but at the expense of an inflammatory response and without significantly enhancing the fraction of hepatocytes entering the cell cycle. These findings unveil aging-dependent replication stress and a crucial role of ATR in mitigating the stress-associated inflammation, a hallmark of aging.

The food and pharmaceutical industries have utilized royal jelly, an alternative medicinal food, as a natural pharmaceutical product since ancient times. Royal jelly has a unique remarkable composition containing lipids, proteins, carbohydrates, vitamins, minerals, hormones, and phenolic compounds. The rapidly expanding functional food market has coincided with the increasing consumer demand for royal jelly. Over the past two decades, royal jelly, a rich source of certain bioactive components, has been used by humans as a functional and nutritious food due to recent studies of the effect of royal jelly in underlying pathogenic processes in a variety of animal models. Scientific evidence has accumulated supporting a wide variety of health-promoting effects from the intake of royal jelly that supports cardiovascular health, immune and antioxidant function, wound healing, blood lipid, and glucose control in addition to antibacterial and antihypertensive effects. The main bioactive ingredients are Major Royal Jelly Proteins (MRJPs), essential oils, fatty acids, peptides, and phenolics, which are thought to have a significant role in the development of honeybee queens. The health-endorsing qualities of royal jelly make it a significant functional ingredient in the food, and cosmetic industry. Apisin is one of the main proteins in royal jelly that has antibacterial properties. Other bioactive ingredients of royal jelly that have multifunctional health-promoting properties include defensin-1, royalisin, apisimin, apidaecin, jelleins, royalactin and 10-hydroxy-2-decenoic acid (10HDA) in epigenetic diseases. This review highlights the important role that royal jelly plays as an agent in various fields of medicine, paying special attention to its biological features. Additionally, we discuss royal jelly's composition as a possible therapeutic for vital natural sources of bioactive substances.

The human glycosylase OGG1 extrudes and excises the oxidized DNA base 8-oxoguanine (8-oxoG) to initiate base excision repair and plays important roles in many pathological conditions such as cancer, inflammation, and neurodegenerative diseases. Previous structural studies have used a truncated protein and short linear DNA, so it has been unclear how full-length OGG1 operates on longer DNA or on nucleosomes. Here we report cryo-EM structures of human OGG1 bound to a 35-bp long DNA containing an 8-oxoG within an unmethylated Cp-8-oxoG dinucleotide as well as to a nucleosome with an 8-oxoG at super-helical location (SHL)-5. The 8-oxoG in the linear DNA is flipped out by OGG1, consistent with previous crystallographic findings with a 15-bp DNA. OGG1 preferentially binds near dsDNA ends at the nucleosomal entry/exit sites. Such preference may underlie the enzyme's function in DNA double-strand break repair. Unexpectedly, we find that OGG1 bends the nucleosomal entry DNA, flips an undamaged guanine, and binds to internal nucleosomal DNA sites such as SHL-5 and SHL+6. We suggest that the DNA base search mechanism by OGG1 may be chromatin context-dependent and that OGG1 may partner with chromatin remodelers to excise 8-oxoG at the nucleosomal internal sites.

Hydroxamic acids represent a group of weak organic acids, both naturally occurring and synthetically derived, characterized by the general formula RC(= O)N(R'OH). In this study, we investigated the binding behavior of N-m-tolyl-4-chlorophenoxyaceto hydroxamic acid with calf thymus DNA (ct-DNA) and torula yeast RNA (t-RNA) through a combination of techniques including UV-visible spectroscopy, fluorescence emission analysis, viscometry, and computational simulations using AutoDock4 software. Our findings reveal that the mode of binding between the compound and the nucleic acids is consistent with intercalation. Competitive binding experiments demonstrated that the complex competes effectively with ethidium bromide (EB) for binding to ct-DNA/t-RNA, displacing EB from its binding sites. Additionally, the introduction of the compound into the DNA-EB system resulted in a quenching of fluorescence emission peaks. Analysis of absorption spectra indicated a red shift and hypochromic shift when the compound interacted with DNA, further supporting the intercalative binding mode. The calculated binding constant (Kb) value for the compound is 6.62 × 104 M-1 and 5.40 × 103 M-1 indicating a strong interaction with ct-DNA and t-RNA respectively. We determined the Stern-Volmer constants for ct-DNA and t-RNA as 9.96 × 104 M-1 and 8.13 × 105 M-1, respectively. The binding free energy values for ct-DNA/t-RNA were calculated to be - 3.741 × 107 and - 5.425 × 108 kcal/mol, respectively. Viscometric studies corroborated the UV results, showing a continuous increase in relative viscosity of ct-DNA/t-RNA solutions with the addition of the optimal hydroxamic acid concentration. Furthermore, we assessed the antioxidant activity of the compound using DPPH-radical scavenging and β-carotene linoleic acid assays. Gel electrophoresis results demonstrated the compound's remarkable efficacy in preventing DNA damage. Collectively, all experimental evidence supports the conclusion that N-m-tolyl-4-chlorophenoxyaceto hydroxamic acid binds to ct-DNA/t-RNA through an intercalative mechanism, which is consistent with our molecular docking simulations.

Low-frequency electromagnetic fields have grown exponentially in recent years due to technological development and modernization. The World Health Organization (WHO)/International Agency for Research on Cancer (IARC) has classified radiofrequency electromagnetic fields (RF-EMFs) as possibly carcinogenic to humans (Group 2B), and recent studies have investigated the association between exposure to electromagnetic fields in parents and possible health effects in children, especially the development of tumours of the central nervous system (CNS). The objective of this systematic review was to collate all evidence on the relationship between parental occupational exposure to electromagnetic fields and the development of CNS cancer in children and to evaluate this association. This review was prepared according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. PubMed, Embase, and Web of Science were searched from January 1990 to April 2021. The search was conducted using the following search string: "occupational" AND "child" AND "electromagnetic" AND "cancer". Seventeen articles met our inclusion criteria: 13 case-control studies, two cohort studies, and 2 meta-analyses. Most of the studies showed several methodological weaknesses that limited their results. Due to a lack of consistency regarding the outcome as well as the heterogeneity in the reviewed studies, the body of evidence for the effects of parental exposure to electromagnetic fields is not clear. Methodological heterogeneity in the way that studies were conducted could be responsible for the lack of consistency in the findings. Overall, the body of evidence allows no conclusion on the relationship between parental exposure to electromagnetic fields and the occurrence of CNS tumours in children.

This study presents the metabolomic profiles of the four Ribes species (Ribes pauciflorum Turcz., Ribes triste Pall., Ribes dicuscha Fisch., and Ribes aureum Purch.). The plant material was collected during two expeditions in the Russian Far East. Tandem mass spectrometry was used to detect target analytes. A total of 205 bioactive compounds (155 compounds from polyphenol group and 50 compounds from other chemical groups) were tentatively identified from the berries and extracts of the four Ribes species. For the first time, 29 chemical constituents from the polyphenol group were tentatively identified in the genus Ribes. The newly identified polyphenols include flavones, flavonols, flavan-3-ols, lignans, coumarins, stilbenes, and others. The other newly detected compounds in Ribes species are the naphthoquinone group (1,8-dihydroxy-anthraquinone, 1,3,6,8-tetrahydroxy-9(10H)-anthracenone, 8,8'-dihydroxy-2,2'-binaphthalene-1,1',4,4'-tetrone, etc.), polyhydroxycarboxylic acids, omega-3 fatty acids (stearidonic acid, linolenic acid), and others. Our results imply that Ribes species are rich in polyphenols, especially flavanols, anthocyanins, flavones, and flavan-3-ols. These results indicate the utility of Ribes species for the health and pharmaceutical industry.

This review is focused on the effects of lingonberry (Vaccinium vitis-idaea L.) fruit phenolic compounds in human in vitro cells and in vivo clinical studies. Studies with lingonberries, lingonberry juice/lingonberry nectar/fermented lingonberry juice, and phenolic fractions with active molecules are reviewed. Lingonberry's bioactive substances have a diverse range of antimicrobial, anti-inflammatory, antiproteolytic, anticancer, and antioxidant properties. Fermentation of lingonberries and modulation of the dysbiotic microbiome to a more symbiotic composition by favoring the growth of lactobacilli and inhibiting the growth of human opportunistic pathogens are discussed. Research results suggest that more studies on humans are needed.

Mitochondrial DNA (mtDNA) is a unique genetic material characterized by maternal inheritance. It possesses a circular structure devoid of histone protection and exhibits low cellular abundance, which poses great challenges for its sensitive and selective detection at the living cell level. Herein, we have designed three bis-naphthylimide probes with varying linker lengths (NANn-OH, n = 0, 2, 6), facilitating the formation of distinct twisted or folded molecular conformations in the free state. These probes emit the red fluorescence around 627 nm with different fluorescence quantum yields (ΦNAN0-OH = 0.0016, ΦNAN2-OH = 0.0136, and ΦNAN6-OH = 0.0125). When encountering mtDNA (0.4-3.4 μg/mL), these probes undergo conformational changes depending on the length of the attached C-strand and exhibit a gradually increasing fluorescence signal around 453 nm. The fluorescence intensity increased to 13.5-fold, 1.9-fold, and 8.2-fold, respectively. Notably, the red fluorescence intensities around 627 nm remain constant throughout this process, thus serving as an inherent correction mechanism for proportional fluorescence signal enhancement to improve selectivity and sensitivity. NAN0-OH, NAN2-OH, and NAN6-OH showed good linearity for mtDNA in the range of 0.4-3.4 μg/mL with detection limits of LODNAN0-OH = 1.04 μg/mL, LODNAN2-OH = 1.10 μg/mL, and LODNAN6-OH = 1.15 μg/mL. Cellular experiments reveal that NAN6-OH effectively monitors curcumin-induced mtDNA damage in HepG-2 cells while enabling monitoring of genetic mtDNA damage. We anticipate that this tool holds significant potential for the precise evaluation of maternal genetic defects, thereby enhancing hypersensitive assessment in clinical medicine.

This work reports the development of low-cost and rapid multiplexed colorimetric assay of antioxidants (total phenolics, antioxidant capacity, flavonoids and anthocyanins) in wines at daisy-shaped fluidic paper-based analytical devices (PADs). The desired fluidic patterns were formed on paper by pen drawing and colorimetric reagents were immobilized at the 6 peripheral test zones. The sample was added at the central sample zone, migrated to the test zones and reacted with the immobilized reagents producing characteristic colors that were captured and analyzed. The paper-based approach was applied to the analysis of several wine samples and the results were statistically correlated to standard solution-based colorimetric assays, indicating that it could be reliably used for ranking wines according to their antioxidants content. In addition, the paper-based analytical methodology is simple, instrument-free, portable, cost-effective, rapid and environment friendly.

Methylene Blue (MB) is an industrial chemical used in a broad range of applications, and hence its discharge is a concern. Yet, the environmental effects of its degradation by HO˙ radicals have not been fully studied yet. This study employs quantum chemical calculations to investigate the two-step degradation of MB by HO˙ radicals in aqueous environments. It was found that MB undergoes a rapid reaction with the HO˙ radical, with an overall rate constant of 5.51 × 109 to 2.38 × 1010 M-1 s-1 and has a rather broad lifetime range of 11.66 hours to 5.76 years in water at 273-383 K. The calculated rate constants are in good agreement with the experimental values (k calculation/k experimental = 2.62, pH > 2, 298 K) attesting to the accuracy of the calculation method. The HO˙ + MB reaction in water followed the formal hydrogen transfer and radical adduct formation mechanisms, yielding various intermediates and products. Based on standard tests these intermediates and some of the products can pose a threat to aquatic organisms, including fish, daphnia, and green algae, they have poor biodegradability and have the potential to induce developmental toxicity. Hence MB in the environment is of moderate concern depending on the ratio of safe to harmful breakdown products.

To examine how the neutrophil-to-lymphocyte ratio (NLR) affects both short-term and long-term mortality in individuals with acute respiratory distress syndrome (ARDS).

A retrospective study.

Critical care unit.

A total of 785 patients with ARDS.

There were three groups in the NLR study. A Cox proportional hazards regression model was used to calculate the hazard ratio (HR) between the NLR and 30-day, 90-day, and 1-year mortality.

The 785 patients included 329 women (41.9%) and 456 men (58.1%), with a mean age of 63.4 ± 16.7 years and a mean NLR of 14.2 ± 9.8. The study population was divided into 3 groups based on NLR value. In the unadjusted model, compared to group 1 (NLR <6.0), group 2 (NLR 6.0-11.3) and group 3 (NLR >11.3) had HR values of 1.12 (95% confidence interval [CI], 0.83-1.52) and 2.39 (95% CI, 1.87-3.04), respectively, for 30-day all-cause mortality. This association remained significant after adjusting for potential confounding variables (HR, 1.54; 95% CI, 1.18-2.02), with a statistically significant trend (p = 0.0004) in group 3 (NLR >11.3). A similar effect was seen on both 90-day and 1-year all-cause mortality. The R2 value in a 2-piecewise linear regression was 1.25 (95% CI, 1.06-1.48; p < 0.0001) on the left side of the inflection point (NLR 17.1).

In this retrospective single-center study, the NLR was a potential predictor of both short- and long-term mortality in patients with ARDS and may aid risk stratification.

We propose that intermittent fasting (time-restricted eating), in agreement with the conclusions of other biologists, as revealed in recent publications, promotes the achievement of numerous health benefits including the extension of human and animal lifespans. Background: There is evidence, obtained both with animal model systems and with humans, that intermittent fasting has health benefits. These benefits include extended longevity, weight loss, and counteracting various disease conditions. Such procedures positively influence the benefits of human tissue-specific microbiomes and minimize the consequences of organellar apoptosis. Key Messages: In this review, we attempt to summarize the predominant evidence, published in the scientific literature, relevant to the conclusions that in general, and in many specific instances, intermittent fasting has long-term benefits to animals, including humans, with respect to overall and specific organismal health and longevity.

With neurodegenerative disorders being on the rise, a great deal of research from multiple fields is being conducted in order to further knowledge and propose novel therapeutic interventions. Among these investigations, research on the role of antioxidants in contrasting cognitive decline is putting forward interesting and promising results. In this review, we aim to collect evidence that focused on the role of a variety of antioxidants and antioxidant-rich foods in improving or stabilizing cognitive functions, memory, and Alzheimer's disease, the most common neurodegenerative disorder. Specifically, we considered evidence collected on humans, either through longitudinal studies or randomized, placebo-controlled ones, which evaluated cognitive performance, memory abilities, or the progression level of neurodegeneration. Overall, despite a great deal of variety between study protocols, cohorts of participants involved, neuropsychological tests used, and investigated antioxidants, there is a solid trend that suggests that the properties of antioxidants may be helpful in hampering cognitive decline in older people. Thus, the help of future research that will further elucidate the role of antioxidants in neuroprotection will lead to the development of novel interventions that will take into account such findings to provide a more global approach to treating neurodegenerative disorders.