Securing the evidence in various investigative situations is often associated with trace analysis, including fingerprints or blood groups. However, when classic and conventional methods fail, trace elements, such as copper, zinc, fluorine, and many others found in exceedingly insignificant amounts in organisms, may prove useful and effective.

The presented work reviews articles published between 2003 and 2023, describing the use of trace elements and the analytical methods employed for their analysis in forensic medicine and related sciences.

Trace elements can be valuable as traces collected at crime scenes and during corpse examination, aiding in determining characteristics like the sex or age of the deceased. Additionally, trace elements levels in the body can serve as alcohol or drug poisoning markers. In traumatology, trace elements enable the identification of various instruments and the injuries caused by their use.

Orofacial clefts (OFCs) have been linked to various toxic and essential trace elements (TETEs) worldwide. However, review estimation is absent. Therefore, addressing the hypothesis that TETEs are associated with OFCs is the main area of this review. A systematic literature search was conducted using electronic databases through PubMed, Web of Science, Scopus, Science Direct, and Google Scholar between 2004 and August 2022. The "AND" and "OR" operators were used to make our search results inclusive and restrictive as follows: ("Toxic element*" OR "Heavy metal*") AND ("Toxic element*" OR "Lead OR Arsenic OR Mercury*")) AND ("Essential trace element*" OR "Zinc OR Selenium OR Copper*")) AND ("Orofacial cleft*" OR "Cleft lip*" OR "Cleft palate*") AND ("Infant*" OR "Newborn*" OR "Neonate*")). The presence of toxic elements was linked to the development of OFCs. The results showed that higher levels of toxic elements in various biological sample types were related to increased risks for OFCs. Increased concentrations of essential trace elements (ETEs) lowered the risk of OFCs. Maternal consumption of diets rich in ETEs, including zinc (Zn), selenium (Se), copper (Cu), cobalt (Co), and molybdenum (Mo), was linked to a more pronounced reduction in the risk of OFCs. Based on the findings, it is acceptable to infer that maternal exposure to toxic elements, whether through environmental contaminants or dietary sources, was associated with an elevated risk of OFCs. Furthermore, the study revealed that ETEs exhibited a potential protective role in reducing the incidence of OFCs. This observation highlights the importance of reducing exposure to toxic elements during pregnancy and suggests that optimizing maternal intake of ETEs could be an effective preventive strategy.

There is limited experimental evidence on the biochemical consequences of aluminium (Al) and cadmium (Cd) co-exposures during pregnancy and postnatal life.This study investigated the impacts of perinatal Al chloride (AlCl3) and Cd chloride (CdCl2) co-exposures on neuroendocrine functions in mice offspring during postnatal life. The study comprised of four pregnant experimental groups. Group 1 received AlCl3 (10 mg/kg), group 2 were administered CdCl2 (1.5 mg/kg), while group 3 received both AlCl3 (10 mg/kg) and CdCl2 (1.5 mg/kg) (AlCl3+CdCl2), and group 4 received saline (10 mL/kg) only and served as control group. All experimental animals were chemically exposed once daily from gestation days 7-20. Upon delivery, male pups were regrouped based on maternal chemical exposure on postnatal day 21 (PND 21) and allowed to grow to adulthood until PND 78, after which they were sacrificed for assessment of neuroendocrine markers and histological investigations. There was no statistical significance (p > 0.05) on follicle stimulating hormone, testosterone, estrogen and progesterone, thyroid stimulating hormone, thyroxine (T4) in all treatment groups relative to controls|. However, AlCl3 and AlCl3-CdCl2 significantly (p < 0.05) reduced triiodothyronine (T3) levels, with a profound increase in T3:T4 ratio by AlCl3, and AlCl3+CdCl2 compared to control. Furthermore, pups from pregnant mice treated with CdCl2 and AlCl3+CdCl2 demonstrated increased testicular malondialdehyde concentration with increased catalase activity relative to controls, suggesting oxidative imbalance. In addition, AlCl3, CdCl2, and AlCl3+CdCl2 exposures induced testicular and hypothalamic architectural disruption compared to controls, with marked architectural derangement in the AlCl3+CdCl2 group. Our findings suggest that prenatal co-exposures to Alcl3 and CdCl2 induce testicular and hypothalamic alterations in offspring via a testicular oxidative stress and thyrotoxicosis-dependent mechanisms.

Both excessive alcohol consumption and exposure to high levels of arsenic can lead to neurodegeneration, especially in the hippocampus. Co-exposure to arsenic and alcohol can occur because an individual with an Alcohol Use Disorder (AUD) is exposed to arsenic in their drinking water or food or because of arsenic found directly in alcoholic beverages. This study aims to determine if co-exposure to alcohol and arsenic leads to worse outcomes in neurodegeneration and associated mechanisms that could lead to cell death. To study this, mice were exposed to a 10-day gavage model of alcohol-induced neurodegeneration with varying doses of arsenic (0, 0.005, 2.5, or 10 mg/kg). The following were examined after the last dose of ethanol: (1) microglia activation assessed via immunohistochemical detection of Iba-1, (2) reactive oxygen and nitrogen species (ROS/RNS) using a colorimetric assay, (3) neurodegeneration using Fluoro-Jade® C staining (FJC), and 4) arsenic absorption using ICP-MS. After exposure, there was an additive effect of the highest dose of arsenic (10 mg/kg) in the dentate gyrus of alcohol-induced FJC+ cells. This additional cell loss may have been due to the observed increase in microglial reactivity or increased arsenic absorption following co-exposure to ethanol and arsenic. The data also showed that arsenic caused an increase in CYP2E1 expression and ROS/RNS production in the hippocampus which could have independently contributed to increased neurodegeneration. Altogether, these findings suggest a potential cyclical impact of co-exposure to arsenic and ethanol as ethanol increases arsenic absorption but arsenic also enhances alcohol's deleterious effects in the CNS.

The multifactorial etiology of major depressive disorder (MDD) includes biological, environmental, genetic, and psychological aspects. Recently, there has been an increasing interest in metallomic studies in psychiatry, aiming to evaluate the role of chosen trace elements in the MDD etiology as well as the progression of symptoms. This narrative review aims to summarize the available literature on the relationship between the concentration of chosen elements in the serum of patients with MDD and the onset and progression of this psychiatric condition. The authors reviewed PubMed, Web of Science, and Scopus databases searching for elements that had been investigated so far and further evaluated them in this paper. Ultimately, 15 elements were evaluated, namely, zinc, magnesium, selenium, iron, copper, aluminium, cadmium, lead, mercury, arsenic, calcium, manganese, chromium, nickel, and phosphorus. The association between metallomic studies and psychiatry has been developing dynamically recently. According to the results of current research, metallomics might act as a potential screening tool for patients with MDD while at the same time providing an assessment of the severity of symptoms. Either deficiencies or excessive amounts of chosen elements might be associated with the progression of depressive symptoms or even the onset of the disease among people predisposed to MDD.

The anthropogenic environment and diet introduce many metals into the human body, both essential and toxic. Absorption leads to systemic exposure and accumulation in body fluids and tissues. Both excess and deficiency of trace elements are health hazards. The primary aim of the present study was to evaluate the concentration of 51 elements in liver samples and 11 selected brain regions obtained at post-mortem examination from a population of adults living in south-eastern Poland (n = 15). A total of 180 analyses were performed by inductively coupled plasma mass spectrometry in two independent replicates. The collected data show very high individual variability in the content of the investigated elements. Macroelements such as sodium, magnesium, phosphorus, potassium, calcium, iron, and zinc occurred in the highest concentrations and with the greatest statistically significant variations. Although the elemental content of the brain and liver differed significantly, the strongest positive correlation between liver and polus frontalis was observed for the essential element selenium (0.9338) and the strongest negative one for manganese (-0.4316) and lanthanum (-0.5110). The brain areas studied have different requirements for phosphorus, manganese, iron, and molybdenum. In addition, males had a significantly (p < 0.05) higher brain content of lanthanides and actinides than females. The results of this study show that the inhabitants of south-eastern Poland are exposed to a fairly uniform accumulation of aluminum and vanadium in the brain, which have the highest affinity to the thalamus dorsalis. This result proves that there is environmental exposure to these elements.

Aluminium (Al) is the most ubiquitous metal in the Earth's crust. Even though its toxicity is well-documented, the role of Al in the pathogenesis of several neurological diseases remains debatable. To establish the basic framework for future studies, we review literature reports on Al toxicokinetics and its role in Alzheimer's disease (AD), autism spectrum disorder (ASD), alcohol use disorder (AUD), multiple sclerosis (MS), Parkinson's disease (PD), and dialysis encephalopathy (DE) from 1976 to 2022. Despite poor absorption via mucosa, the biggest amount of Al comes with food, drinking water, and inhalation. Vaccines introduce negligible amounts of Al, while the data on skin absorption (which might be linked with carcinogenesis) is limited and requires further investigation. In the above-mentioned diseases, the literature shows excessive Al accumulation in the central nervous system (AD, AUD, MS, PD, DE) and epidemiological links between greater Al exposition and their increased prevalence (AD, PD, DE). Moreover, the literature suggests that Al has the potential as a marker of disease (AD, PD) and beneficial results of Al chelator use (such as cognitive improvement in AD, AUD, MS, and DE cases).

To evaluate the risk of cognitive impairment in workers with plasma aluminum concentrations and lifestyles using a Bayesian network (BN).

In 2019, 476 male workers in the Shanxi Aluminum factory were investigated. We measured plasma aluminum concentrations in workers by inductive coupled plasma mass spectrometry (ICPMS) and tested workers' cognitive function by the MoCA scale. We collected the data of lifestyle by the occupational Workers' Health questionnaire and express the influence of lifestyle on cognition by the OR value (95 %CI) of logistic regression. A Bayesian network model was used to predict the risk of cognitive dysfunction.

The subjects were divided into a cognitively normal group and cognitively impaired group according to MoCA scores. There were statistically significant differences in age, education level, alcohol consumption, physical exercise, reading, aluminum length of service and blood aluminum concentration between the two groups (P < 0.05). The plasma aluminum concentration in the cognitive impairment group was 1.68 times higher than that in the cognitive normal group. Four groups were established according to the quartile of blood aluminum concentration of the subjects, namely, Group Q1 (<14.95 μg/L), Q2 group (14.95-32.96 μg/L), Q3 group (32.96-56.62 μg/L), and Q4 group (>56.62 μg/L). Binary logistic regression analysis showed that in the adjustment variable Model2, drinking, short sleep, long sleep, and mobile phone use increased the risk of cognitive impairment by 1.505(0.99,2.289), 1.269(0.702,2.295), 1.125(0.711,1.781) and 1.19(0.779,1.82), respectively, compared with their reference values. The risk of cognitive impairment from reading and exercise was 0.7(0.398,1.232) and 0.787(0.51,1.217), respectively, compared with those of no reading and no exercise. The risk of cognitive impairment of blood aluminum concentration in the Q2, Q3, and Q4 groups was 2.103(1.092,4.051), 1.866(0.955,3.644) and 3.679(1.928,7.020), respectively, compared with that in the Q1 group. Compared with age <40 , the risk of cognitive impairment of age ≥40 was 2.515(1.508,4.193) (P < 0.05). Bayesian network model results showed that if all participants had plasma aluminum concentrations higher than Q4, the prevalence of cognitive impairment was 54.5 %. The prevalence of cognitive impairment was 75.0 % if all participants had plasma aluminum levels above Q4, were older than 40, smoked, drank alcohol, used a cell phone for more than 2 h, slept for more than 8 h, did not exercise, and did not read.

Our findings suggest that both poor lifestyle and occupational aluminum exposure may affect cognitive function. Workers must maintain a reasonable lifestyle and reduce aluminum exposure, which can control the occurrence of cognitive impairment.

Aluminum (Al) is linked to the development of many neurological disorders such as Alzheimer's disease (AD), Parkinson's disease, and autism. Centella asiatica (CA) is a regenerating herb traditionally used to stimulate memory. This study was designed to assess the neuroprotective role of ethanolic extract of CA (CAE) in AlCl₃-induced neurological conditions in rats. Adult rats were chronically treated with AlCl₃ (100 mg/kg b.w./day) for 60 days to establish the dementia model, and co-administration of CAE was evaluated for its ability to attenuate the toxic effect of AlCl₃. CAE was given orally at a dose of 150 and 300 mg/kg b.w./day, for 60 days. The behavioral performances of rats were tested through Y-maze and open field tests. Lipid peroxidation, superoxide dismutase, and catalase activity were evaluated to measure oxidative stress; and acetylcholinesterase (AChE) activity was assessed to evaluate cholinergic dysfunction in the rat brain. H&E staining was used to assess structural abnormalities in the cortex and hippocampus. The result showed that AlCl₃ induces cognitive dysfunction (impaired learning and memory, anxiety, diminished locomotor activity), oxidative stress, cholinergic impairment, and histopathological alteration in the rat brain. Co-administration of CAE with AlCl₃ markedly protects the brain from AlCl₃-induced cognitive dysfunction, oxidative stress, AChE activity, and cytoarchitectural alterations. Furthermore, 15 days CAE treatment after 45 days AlCl₃ administration markedly ameliorates the AlCl₃-induced neurotoxicity indicating its potential for therapeutic use.

Metals perform many important physiological functions in the human body. The distribution of elements in different tissues is not uniform. Moreover, some structures can be the site of an accumulation of essential or toxic metals, leading to multi-directional intracellular damage. In the nervous system, these disorders are especially dangerous. Metals dyshomeostasis has been linked to a variety of neurological disorders which end up leading to permanent injuries. The multi-elemental composition of the human brain is still the subject of numerous investigations and debates. In this study, for the first time, the meninges, i.e., the dura mater and the arachnoid, were examined for their elemental composition by means of inductively coupled plasma mass spectrometry (ICP-MS). Tissue samples were collected post mortem from those who died suddenly as a result of suicide (n = 20) or as a result of injuries after an accident (n = 20). The interactions between 51 elements in both groups showed mainly weak positive correlations, which dominated the arachnoid mater compared to the dura mater. The study showed differences in the distribution of some elements within the meninges in the studied groups. The significant differences concerned mainly metals from the lanthanide family (Ln), macroelements (Na, K, Ca, Mg), a few micronutrients (Co), and toxic cadmium (Cd). The performed evaluation of the elemental distribution in the human meninges sheds new light on the trace metals metabolism in the central nervous system, although we do not yet fully understand the role of the human meninges.

Trace element accumulation varies in different human tissues. Distribution of several elements was found to be disrupted in the case of excessive alcohol consumption, causing negative effects and exacerbation of pathological processes in the liver. In this study, we analyzed the levels and interactions between seven trace elements including calcium (Ca), cobalt (Co), chromium (Cr), copper (Cu), iron (Fe), potassium (K), and magnesium (Mg), manganese (Mn), sodium (Na), zinc (Zn), and selenium (Se) in individuals with alcohol-use disorder (AUD) and patients without AUD (control group). The liver samples were collected during autopsy from 39 individuals with AUD and 45 control subjects. Elemental composition inductively coupled plasma optical emission spectrometry (ICP-OES) after wet mineralization by nitric acid was applied for the evaluation of the samples. Positive correlations dominated in the AUD group, mainly in relation to Mg, which strongly positively correlated with Ca, Mn, Fe; K correlated with Mn and Zn, and Cu positively correlated with K and Zn. The strongest positive correlation in the AUD group was observed for the Mg-Mn pair (r = 0.87). Significant statistical differences (p < 0.05) between the groups concerned the average concentration of Co, Cu, Mn, and Mg, which were lower in the AUD group, and Fe, the level of which was significantly higher in the AUD group compared to the control group. Evaluation of the chronic alcohol consumption effect on the accumulation of trace elements in the liver allows a better understanding of the pathological processes taking place in this organ.

The identification of biomarkers as diagnostic tools and predictors of response to treatment of neurological developmental disorders (NDD) such as schizophrenia (SZ), attention deficit hyperactivity disorder (ADHD), or autism spectrum disorder (ASD), still remains an important challenge for clinical medicine. Metallomic profiles of ASD patients cover, besides essential elements such as cobalt, chromium, copper, iron, manganese, molybdenum, zinc, selenium, also toxic metals burden of: aluminum, arsenic, mercury, lead, beryllium, nickel, cadmium. Performed studies indicate that children with ASD present a reduced ability of eliminating toxic metals, which leads to these metals' accumulation and aggravation of autistic symptoms. Extensive metallomic studies allow a better understanding of the importance of trace elements as environmental factors in the pathogenesis of ASD. Even though a mineral imbalance is a fact in ASD, we are still expecting relevant tests and the elaboration of reference levels of trace elements as potential biomarkers useful in diagnosis, prevention, and treatment of ASD.

Some trace elements (TE) are eminently toxic for humans (e.g., Al, Pb, Hg, Cd) and its presence in the central nervous system has been linked to the etiology of neurodegenerative diseases (ND). More recently, the focus has shifted to the potential role of the imbalances on essential TE levels (e.g., Fe, Cu, Zn, Se) within the brain tissue, and they have also been identified as potentially responsible for the cognitive decline associated with normal ageing and the development of some ND, although their definite role remains unclear. Accurately, well-defined reference values for TE levels in human body fluids and tissues are indispensable to identify possible disturbances in individual cases. Moreover, since the brain is a highly heterogeneous organ, with anatomically and physiologically very different areas, a detailed mapping of TE distribution across the brain tissue of normal individuals, with an in-depth analysis of TE levels in the different brain regions, is a mandatory prior work so that the results obtained from patients suffering from ND and other brain diseases can be interpreted. This review aims to compile and summarize the available data regarding TE levels in the different human brain regions of "normal" (non-diseased) individuals in order to contribute to the establishment of robust reference values. Fifty-four studies, published since 1960, were considered. The results showed a great variability between different studies. The potential sources of this variability are discussed. The need for increased harmonization of experimental strategies is highlighted in order to improve the comparability of the data obtained.

The alterations in serum trace element levels are common phenomena observed in patients with different psychiatric conditions such as schizophrenia, autism spectrum disorder, or major depressive disorder. The fluctuations in the trace element concentrations might act as potential diagnostic and prognostic biomarkers of many psychiatric and neurological disorders. This paper aimed to assess the alterations in serum trace element concentrations in patients with a diagnosed schizophrenia. The authors made a systematic review, extracting papers from the PubMed, Web of Science, and Scopus databases according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Among 5009 articles identified through database searching, 59 of them were assessed for eligibility. Ultimately, 33 articles were included in the qualitative synthesis. This review includes the analysis of serum levels of the following trace elements: iron, nickel, molybdenum, phosphorus, lead, chromium, antimony, uranium, magnesium, aluminum, zinc, copper, selenium, calcium, and manganese. Currently, there is no consistency regarding serum trace element levels in schizophrenic patients. Thus, it cannot be considered as a reliable prognostic or diagnostic marker of schizophrenia. However, it can be assumed that altered concentrations of those elements are crucial regarding the onset and exaggeration of either psychotic or negative symptoms or cognitive dysfunctions.

Gastric cancer (GC) is undoubtedly one of the most prevalent malignancies worldwide. Since GC is the second leading cause of cancer-related deaths with nearly one million new diagnoses reported every year, there is a need for the development of new, effective treatment strategies of GC. Gastric carcinogenesis is a complex process that is induced by numerous factors and further stimulated by many pro-oncogenic pathways. Angiogenesis is the process of the new blood vessels formation from the already existing ones and it significantly contributes to the progression of gastric tumorigenesis and the growth of the cancerous tissues. The newly formed vessels provide cancer cells with proper nutrition, growth factors, and oxygen supply that are crucial for tumor growth and progression. Tumor-associated vessels differ from the physiological ones both morphologically and functionally. They are usually inefficient and unevenly distributed due to structural transformations. Thus, the development of the angiogenesis inhibitors that possess therapeutic effects has been the main focus of recent studies. Angiogenesis inhibitors mostly affect the vascular endothelial growth factor (VEGF) pathway since it is a major factor that stimulates the pro-angiogenic pathways. The aim of this review was to describe and summarize other promising molecular pathways that might be crucial in further improvements in GC therapies. This article provides an overview of how a meaningful role in tumor progression the angiogenetic process has. Furthermore, this review includes a description of the most important angiogenic factors as well as pathways and their involvement in gastric carcinogenesis.

Macronutrients and trace elements are important components of living tissues that have different metabolic properties and functions. Trace elements participate in the regulation of immunity through humoral and cellular mechanisms, nerve conduction, muscle spasms, membrane potential regulation as well as mitochondrial activity and enzymatic reactions. Excessive alcohol consumption disrupts the concentrations of crucial trace elements, also increasing the risk of enhanced oxidative stress and alcohol-related liver diseases. In this review, we present the status of selected macroelements and trace elements in the serum and plasma of people chronically consuming alcohol. Such knowledge helps to understand the mechanisms of chronic alcohol-use disorder and to progress and prevent withdrawal effects, also improving treatment strategies.

There is limited information on whether metals such as aluminum (Al) can migrate from orthodontic braces to saliva and subsequently contribute to its exposure in humans. This study aimed to assess this experimentally by incubating elastomeric orthodontic ligatures in artificial saliva for 30 days and other components of orthodontic braces (brackets, arch wires, and retainers) up to 180 days. As demonstrated, significantly higher levels of Al were leached from elastomeric ligatures (mean ± SD 28.2 ± 6.8 μg compared with their stainless steel counterparts (3.6 ± 0.1 μg) during 30 days. The higher the incubation time, the greater levels of Al leaching to artificial saliva were observed with the highest levels found for CNA β arch wire (252 ± 12 μg), Ni-Ti-Al arch wire (224 ± 11 μg), ceramic brackets (199 ± 10 μg), stainless steel arch wire (108 ± 5 μg), and metallic brackets (81.0 ± 4.2 μg) after 180 days of incubation. However, considering the tolerable weekly intake (TWI) established by the European Food Safety Authority, the intraoral use of orthodontic braces considered in this study would in the worst case constitute 0.04% and 0.09% of TWI in 70-kg adults and 30-kg children, respectively. In conclusion, the orthodontic braces considered in this study have no contribution to Al exposure in humans and can be considered safe in this regard.

Agaricus bisporus is the most commonly cultivated and consumed mushroom species. The aim of this study was to compare the profile of macro- and trace elements in A. bisporus fruit bodies produced commercially in 19 countries in 2018 and distributed worldwide (32 analyzed objects). Trace elements with unknown biological roles were also determined. The content of 36 elements (of 70 taken into account) revealed significant differences among the analyzed objects. Contents of Ca, K, Mg, Na and S varied in wide ranges of 425-2430, 12740-40940, 610-3240, 98-430 and 1030-2650 mg kg^-1 dw, respectively. The fruit bodies were characterized by a generally similar content of trace elements with some clear exceptions. Rankings of the objects according to the decreased amount of macroelements, trace elements and all elements jointly, show that mushrooms are significantly diverse as regards the content of particular elements of the mentioned group. The analyzed fruit bodies displayed a relatively high content of Ca, Mo and Se, and a high K/Na ratio. Regardless of origin, A. bisporus did not constitute a source of significant levels of Al, Cd or rare earth elements. An increased level of As and Pb in mushrooms from several producers indicates a need for additional measures to reduce potential dietary exposures to these toxicants.

Trace elements play an important role in the pathogenesis of several serious ophthalmological disorders, such as glaucoma, age-related macular degeneration (AMD), diabetic retinopathy, cataract, etc. This study aimed to measure alterations of chemical elements' (67) levels in the aqueous humor of patients undergoing cataract surgery. The pilot study included 115 patients, (age 74 ± 7.27, female 64.35%, male 35.65%). The aqueous levels of elements were measured by the use of the inductively coupled plasma optical emission spectrometry (ICP-OES), quality controlled with certified standards. The classification of elements based on their concentration was achieved by hierarchical cluster analysis. This is the first screening study that quantifies over 60 elements which are present in the fluid from the anterior chamber of the eye of cataract patients. The obtained results can be suitable for understanding and identifying the causes that may play a role in the initiation and progression of lens opacity.