Published online Jun 25, 2026. doi: 10.5527/wjn.v15.i2.116474
Revised: December 30, 2025
Accepted: February 12, 2026
Published online: June 25, 2026
Processing time: 215 Days and 15.8 Hours
Testicular ischemia/reperfusion (I/R) injury may affect distant organs. During I/R, metabolites formed in the affected organ are released into the circulation; thus, non-ischemic organs, such as the kidneys and lungs, become involved in the inflammatory process, even if they are not primarily affected. Damage from testicular torsion/detorsion (T/D) models has been shown to affect kidneys. There is a need to examine the nephroprotective effect of boric acid (BA), which is known to have antioxidant effects, on kidney damage.
To investigate kidney damage in a rat testicular T/D model and the effectiveness of BA on this distant organ damage.
Twenty-four male Wistar albino rats were divided into four groups (n = 6 each)-control (group C), BA (group BA), T/D (group I/R), BA-T/D (group BA-I/R). In all groups, the scrotum was cut longitudinally, and the testis was dissected. No medication was administered to groups C and group I/R. Groups BA and group BA-I/R were administered 50 mg/kg BA intraperitoneally half an hour before the surgical procedure. The testicular T/D model was applied to groups I/R and group BA-I/R. The malondialdehyde (MDA) level, catalase, glutathione S-transferase, and paraoxonase-1 (PON-1) enzyme activities were measured in kidney tissue. Additionally, sections were taken and evaluated for histopathological examination.
An increase in MDA levels and a decrease in PON-1 activity were detected in the I/R group compared to the control group (P = 0.001, P = 0.002, respectively). MDA levels were found to be significantly lower in the BA-I/R group than in the I/R group (P = 0.041). PON-1 enzyme activity was found to be significantly higher in the BA-I/R group than in the I/R group (P = 0.048). The light microscopy examination showed an increase in glomerular vacuolization, tubular dilatation, vascular vacuolization and hypertrophy (VVH), and tubular cell degeneration and necrosis damage scores in the I/R group compared to the control group (P = 0.003, P = 0.005, P = 0.008, and P < 0.001, respectively). In the I/R group treated with BA, tubular dilatation and VVH scores decreased compared to the I/R group (P = 0.037 and P = 0.048, respectively).
These findings show that the testicular T/D model in rats causes kidney damage, and BA administration reduces this damage in the kidneys.
Core Tip: Ischemia/reperfusion (I/R) injury is a serious problem that is encountered in several clinical settings. Testicular torsion/detorsion (T/D) is one example. It is known that damage to distant organs can occur following I/R. Significant scientific data and experimental studies demonstrate the antioxidant effects of boric acid (BA), such as increasing antioxidant enzyme levels and reducing oxidative stress. The protective role of BA against potential kidney damage has been investigated. These findings suggest that BA may protect against distant I/R damage from testicular T/D. This may facilitate further research into the use of BA as a treatment for I/R injury.
- Citation: Adam UM, Alkan M, Sezen ŞC, Kavutçu M, Arslan M. Protective effect of boric acid on kidney tissue and oxidative stress after testicular torsion/detorsion in male rats. World J Nephrol 2026; 15(2): 116474
- URL: https://www.wjgnet.com/2220-6124/full/v15/i2/116474.htm
- DOI: https://dx.doi.org/10.5527/wjn.v15.i2.116474
Testicular torsion occurs when the testis rotates and the spermatic cord twists, restricting blood flow to the testis. One in 4000 men under the age of 25 face this condition each year[1]. Early diagnosis and surgical intervention are important to prevent infertility[2]. The aim of treatment is to restore blood flow in ischemia and improve tissue perfusion[3]. Although perfusion returns after detorsion, a pathological condition called ischemia/reperfusion (I/R) injury occurs afterwards[4]. This situation can cause more damage than the damage caused by ischemia through various mechanisms[5].
Overproduction of reactive oxygen species (ROS) during testicular I/R is a major initiating component of testicular injury[6]. The inflammatory response after I/R results in further ROS generation and an increase in the expression of proinflammatory cytokines[7]. ROS reacts with proteins, lipids, carbohydrates, and nucleic acids, causing a disruption in cell function[8]. Injury from I/R results in neutrophil recruitment, lipid peroxidation and apoptosis[9]. Exposure of a single organ to I/R may subsequently cause inflammatory activation in other organs and eventually lead to multiple organ failure[10]. Testicular torsion/detorsion (T/D) causes a significant increase in the level of malondialdehyde (MDA), resulting from lipid peroxidation, and leads to significant reductions in superoxide dismutase (SOD) and catalase (CAT) activities in the ipsilateral testis[4]. Glutathione S-transferase (GST), paraoxonase-1 (PON-1), and CAT enzymes protect the cell’s DNA and lipids against peroxidation products, and monitoring their levels when oxidative stress occurs can give an idea about the amount of damage and antioxidant status[11-13].
Boric acid (BA) has beneficial effects on tumor inhibition, energy metabolism, and hormones in organisms[14]. In recent years, BA has also been shown to have anti-inflammatory and antioxidant effects[15]. Testicular T/D experiments conducted in rats have yielded successful results in the literature and offer some insights into human biology. Therefore, a similar model was designed based on previous studies. Our aim in this study is to determine whether the potential damage that may occur in the kidney after reperfusion in the rat testicular T/D model can be reduced by applying BA.
Wistar albino rats were purchased from the Gazi University Animal Experiments Laboratory (Ankara, Türkiye), where this study was conducted. All experiments were performed in accordance with the standards of the Guide for the Care and Use of Laboratory Animals (National Research Council, 2011). All procedures were reviewed and approved by the Animal Research Committee of Gazi University.
The animal protocol was designed to minimize pain and discomfort for the animals. In the study, 24 male Wistar albino rats, older than 12 months and weighing 250-350 g, were used. The rats were kept in steel cages at a room temperature of 22 °C and were housed on a 12 hours light–dark cycle. Food and water requirements were fulfilled in the form of free feeding, allowed up to 2 hours before the experiment. The rats were randomly divided into four groups, each group containing six animals-control group (Group C), BA group (Group BA), T/D group (Group I/R), BA-torsion/detorsion group (Group BA-I/R)-each group containing six animals. All rats were administered 50 mg/kg intraperitoneal (i.p.) ketamine (Ketax; 500 mg/10 mL, VEM İlaç San. Ve Tic. A.Ş., İstanbul, Türkiye) and 10 mg/kg i.p. xylazine (Alfazyne 20 mg/mL; Ege Vet, İzmir, Türkiye) for anesthesia and analgesia before the procedure. During the surgical procedure, the rats were placed on a heating pad to maintain a constant body temperature. In all groups, asepsis was ensured, and the scrotum was cut longitudinally; additionally, the left testis was dissected. No medication was administered to Groups C and I/R. Groups BA and BA-I/R were administered i.p. 50 mg/kg BA, which was dissolved in 100 mL of distilled water and then diluted to a concentration of 50 mg/kg half an hour before the surgical procedure. The testicular T/D model was applied to Groups I/R and BA-I/R. The left testes of the animals in Groups I/R and BA-I/R were rotated 720° in a clockwise direction and fixed in the torsion position. In these two groups, the testes remained in torsion for 2 hours and then in detorsion for 2 hours. Following the end of the reperfusion period, all rats were anesthetized using ketamine (100 mg/kg) and xylazine (10 mg/kg) i.p. injection, and were sacrificed by exsanguination during blood sample (5-10 mL) collection from the heart. After the heart rate and respiration ceased, monitoring was continued for a further 2 minutes to confirm death. The kidney tissues of all rats were then taken for histopathological and biochemical evaluations. Kidney tissues were placed in a 40 g/L formalin solution for histopathological examination and in liquid nitrogen for biochemical analysis. These samples were stored in a -80 °C freezer. The researchers who performed the biochemical analyses and histopathological scoring were blinded to the group allocations. Analysis of the sections was performed by the same histologist blindly.
Histopathological examination was performed at the Department of Histology and Embryology, Kırıkkale University Faculty of Medicine (Kırıkkale, Türkiye). Kidneys that underwent routine fixation procedures were placed in paraffin blocks, whereby 5 μ sections were made, then stained with hematoxylin and eosin and examined with a light microscope. For histopathological evaluation, the scoring table used by Bostan et al[16] was used. Each kidney sample was evaluated for similar injury criteria for glomerular vacuolization (GV), tubular dilatation (TD), vascular vacuolization and hypertrophy (VVH), tubular cell degeneration and necrosis (TCDN), bowman space dilatation (BSD), tubular hyaline casts (THC), lymphocyte infiltration (LI), and tubular cell shedding (TCS). A 4-point scoring system was used (0: No change, +1: Minimal change, +2: Moderate change, +3: Severe change).
Biochemical examinations were performed in the Research Laboratory of the Department of Medical Biochemistry, Gazi University Faculty of Medicine (Ankara, Türkiye). To investigate oxidative stress and lipid peroxidation in kidney tissues, MDA levels and CAT, GST, and PON-1 enzyme activities, which are active enzymes in free radical metabolism, were measured. Kidney tissues to be used in the experiment were homogenized in 1/7 ratio of saline solution for 1-2 minutes at 4000 g with a Heidolph DIAX900 brand homogenizer. The crude homogenate was centrifuged at 5000 g for 20 minutes, and the supernatants were collected. Supernatants were placed in separate Eppendorf tubes for enzyme and other analyses and stored in a deep freezer at -80 ºC until the day of analysis. All analyses were performed within one week.
MDA analysis was performed according to Van Ye et al[17]. Two moles of thiobarbituric acid (TBA) were combined with one mole of MDA in an acidic environment and at 85-100 ºC to form the pink TBA-MDA complex, and the absorbance of this complex was measured spectrophotometrically at 532 nm. The amount of MDA was calculated using the slope of the standard graph drawn with 1,1,3,3-Tetraethoxy propane used as the MDA standard; the amount of MDA in the samples was calculated from the slope of the absorbance = concentration graph, and the results were given as nanomoles per milligram of protein.
Determination of GST activity was performed according to Habig et al[18]. An increase in absorbance was measured at 340 nm, which could be attributed to a reduction in dinitrophenyl glutathione. The results were expressed as international units per milligram of protein.
CAT activity measurement in samples was done according to the Aebi method[19]. A decrease in absorbance was measured at 240 nm due to H2O2 consumption. The results were expressed as international units per milligram of protein.
The PON-1 enzyme activity was measured according to Furlong et al[20]. Since PON catalyzes the decomposition of paraoxon into p-nitrophenol and acetic acid, the formation of p-nitrophenol results in maximum absorbance at 405 nm. Using this feature, PON activity was measured spectrophotometrically. The results were expressed as international units per milligram of protein.
The protein amount in supernatants was determined according to the Lowry method[21]. The principle of the method is based on the formation of a blue-violet colored product by reducing the phospho molybdate-phospho tungstate reagent (Folin-Ciocalteau-Phenol reagent) by forming a Cu2+-protein complex in an alkaline environment. The darkness of the color is directly proportional to the protein concentration in the medium. In this study, the amount of protein in the samples was calculated using the slope of the standard graph drawn using Bovine Serum Albumin as the protein standard.
The study data were analyzed using the statistical program SPSS (Statistic Program for Social and Science), (SPSS Inc, Chicago, IL, United States). Statistical evaluation was performed using the tests listed below in the SPSS 20.0 computer program, and P < 0.05 was considered significant. Data are presented as mean ± SE.
The Kolmogorov–Smirnov test was applied to the measurable parameters to determine whether the distribution was normal or abnormal. Kruskal-Wallis test followed by Dunn’s post hoc test.
All 24 animals included in the study were examined. When the groups were compared among themselves in terms of MDA levels, a statistically significant difference was observed between the groups (P = 0.002). MDA levels were found to be significantly higher in the group I/R than in the control and BA groups (7.98 ± 0.60 nmol/mg vs 4.78 ± 0.30 nmol/mg protein, P = 0.001, and 7.98 ± 0.60 nmol/mg vs 5.17 ± 0.32 nmol/mg protein, P = 0.023, respectively). In addition, MDA levels were found to be significantly lower in the group BA-I/R than in the group I/R (5.90 ± 0.59 nmol/mg vs 7.98 ± 0.60 nmol/mg protein, P = 0.041). When the groups were compared among themselves in terms of PON-1 enzyme activity, there was a significant difference between the groups (P = 0.010). PON-1 enzyme activity was found to be significantly lower in the group I/R compared to the control and group BA (1.69 ± 0.13 IU/mg vs 2.74 ± 0.24 IU/mg protein, P = 0.002, 1.69 ± 0.13 IU/mg vs 2.50 ± 0.13 IU/mg protein, P = 0.007, respectively). In addition, the result in the group BA-I/R was significantly higher than in the group I/R (2.25 ± 0.17 IU/mg vs 1.69 ± 0.13 IU/mg protein, P = 0.048). When the groups were compared in terms of GST and CAT enzyme activity, no significant differences were found between the groups (P = 0.111, P = 0.637, respectively) (Table 1).
| Group control (n = 6) | Group BA (n = 6) | Group I/R (n = 6) | Group BA-I/R (n = 6) | aP value | |
| GST (IU/mg protein) | 1.90 ± 0.44 | 2.04 ± 0.08 | 1.45 ± 0.13 | 1.62 ± 0.18 | 0.111 |
| CAT (IU/mg protein) | 4192 ± 276 | 3797 ± 558 | 3610 ± 432 | 3810 ± 438 | 0.637 |
| PON-1 (IU/mg protein) | 2.74 ± 0.24 | 2.50 ± 0.13 | 1.69 ± 0.13b,c | 2.25 ± 0.17d | 0.010 |
| MDA (nmol/ mg protein) | 4.78 ± 0.30 | 5.17 ± 0.32 | 7.98 ± 0.60b,c | 5.90 ± 0.59d | 0.002 |
In light microscopy, the GV damage score was found to be significantly different between the groups (P = 0.008). It was higher in the group I/R compared to the control and group BA (1.33 ± 0.21 vs 0.17 ± 0.17, P = 0.003, and 1.33 ± 0.21 vs 0.33 ± 0.21, P = 0.012, respectively). It was higher in the group BA-I/R compared to the control group (1.00 ± 0.26 vs 0.17 ± 0.17, P = 0.028). TD was found to be significantly different between the groups (P = 0.007), increasing in the group I/R compared to the control and group BA (1.83 ± 0.17 vs 0.50 ± 0.22, P = 0.005, and 1.83 ± 0.17 vs 0.33 ± 0.21 P = 0.001, respectively). In addition, TD was significantly lower in the group BA-I/R than in the group I/R (0.83 ± 0.31 vs 1.83 ± 0.17, P = 0.037). VVH was found to be significantly different between the groups (P = 0.025). It was higher in the group I/R compared to the control and group BA (1.33 ± 0.21 vs 0.33 ± 0.21, P = 0.008, and 1.33 ± 0.21 vs 0.33 ± 0.21 P = 0.008, respectively). In addition, it was found to be significantly lower in the group BA-I/R than in the group I/R (0.67 ± 0.21 vs 1.33 ± 0.21, P = 0.048). The TCDN was found to be significantly different between the groups (P = 0.005). It was higher in the group I/R compared to the control and BA groups (1.00 ± 0.00 vs 0.00 ± 0.00, P < 0.001, and 1.00 ± 0.00 vs 0.33 ± 0.21, P = 0.024, respectively). LI, THC, BSD, and TCS were found to be similar among the groups (P = 0.295, P = 0.113, P = 0.133, and P = 0.350, respectively) (Figure 1 and Table 2).
| Group control (n = 6) | Group BA (n = 6) | Group I/R (n = 6) | Group BA-I/R (n = 6) | aP value | |
| GV | 0.17 ± 0.17 | 0.33 ± 0.21 | 1.33 ± 0.21b,c | 1.00 ± 0.26b | 0.008 |
| TD | 0.50 ± 0.22 | 0.33 ± 0.21 | 1.83 ± 0.17b,c | 0.83 ± 0.31d | 0.007 |
| VVH | 0.33 ± 0.21 | 0.33 ± 0.21 | 1.33 ± 0.21b,c | 0.67 ± 0.21d | 0.025 |
| TCDN | 0.00 ± 0.00 | 0.33 ± 0.21 | 1.00 ± 0.00b,c | 0.50 ± 0.21 | 0.005 |
| BSD | 0.33 ± 0.21 | 0.50 ± 0.22 | 1.00 ± 0.26 | 0.50 ± 0.34 | 0.295 |
| THC | 0.33 ± 0.21 | 0.50 ± 0.22 | 1.00 ± 0.00 | 0.67 ± 0.21 | 0.113 |
| LI | 0.50 ± 0.22 | 0.50 ± 0.22 | 1.17 ± 0.17 | 0.67 ± 0.21 | 0.133 |
| TCS | 0.33 ± 0.21 | 0.50 ± 0.22 | 0.83 ± 0.17 | 0.67 ± 0.21 | 0.335 |
Although I/R injury occurs primarily locally, damage may subsequently develop in distant organs[22,23]. Systemic effects are observed predominantly in the heart, brain, lung, liver, and kidney[24-26]. Kidneys are particularly vulnerable to I/R injury[27]. Several studies in the literature show distant organ I/R damage accompanied by renal involvement[22-26]. There are limited reports investigating distant organ injury following testicular I/R injury. In an experiment using the testicular torsion model, testicular I/R caused an increase in the level of oxidative stress in the lung tissue of rats[28]. In a study conducted in rats by Bozlu et al[29], they found that no damage occurred in the distant organ, the kidney, after testicular I/R injury. Another testicular T/D experiment conducted by Ozdemirkan et al[30] showed that antioxidant enzyme levels (CAT, PON-1, GST) were low, MDA levels were high, and histopathological damage occurred in lung and kidney tissues.
Various therapeutic agents have been tried in the literature to reduce I/R damage. These chemicals often have anti-inflammatory, antioxidant, or ROS-scavenging properties. ROS scavengers, such as N-acetylcysteine, have been found to protect against I/R injury in animals[31]. Additionally, modafinil[32], sildenafil[33], erythropoietin[33], rutin[4], α-lipoic acid[34], dexamethasone[35], poly (adenosine diphosphate-ribose) polymerase inhibitors[29], and cerium oxide[30] have been investigated as protective agents against I/R injury.
Similar to all these studies, BA has been shown to have protective and antioxidant effects in recent years[36-40]. A number of articles have shown that boron promotes free radical scavenging by increasing the activities of antioxidant enzymes, including SOD, CAT, GST, and glutathione peroxidase (GPx) in the blood and cells[15,38,41]. Boron has also been proven to reduce levels of inflammatory biomarkers, such as tumor necrosis factor-alpha, high-sensitivity C-reactive protein, and interleukin-6[15]. Administration of BA has also been shown to inhibit apoptotic activity after renal I/R[42]. All of these effects provide strong evidence that BA reduces the harmful effects of I/R damage on tissues.
Although the protective effect of BA on local organ damage has been experimentally demonstrated, its effects on distant organs in I/R damage have recently begun to be investigated[39,43,44]. Examples where local organ damage from I/R and other sources of oxidative stress is reduced by BA have been shown in the liver[45,46], brain[40], kidney[42,47-50], lung[51], heart[52], and ovary[53]. However, to our knowledge, no study has been conducted on the effect of BA on distant organ damage after testicular I/R.
The study conducted by Ozek et al[43] on distant organ I/R determined that BA has a protective effect against liver damage caused by renal I/R. Another study has shown that administration of BA after establishing a renal I/R model can protect against I/R injury by regulating pancreatic functions[39]. In the study conducted by Özcan et al[44], the effects of BA in preventing lung damage as a result of lower extremity I/R in rats were investigated, and an increase in antioxidant enzyme activity (SOD, CAT, GPx) and normalization in histopathological findings were detected in the lung tissue after BA application.
Distinctive morphological features of acute kidney injury include effacement and loss of the proximal tubule brush border, loss of cell polarity, patchy loss of tubule cells, dilatation of the proximal tubules, and areas of distal tubular debris and cellular regeneration. Additionally, vascular occlusion, endothelial damage, and leukocyte accumulation may be found in peritubular capillaries[54,55]. In our own study, histopathological examinations performed on kidney tissue revealed significantly higher levels of GV, TD, VVH, and, finally, TCDN scores in the I/R group. The elevation of these parameters is compatible with morphological changes in the kidneys in acute kidney injury. However, the lack of significant change in some of the parameters examined, such as BSD, THC, LI, and TCS, led us to question the level of renal damage that may occur after testicular I/R. In the I/R group pretreated with BA, a significant improvement was found in TD and VVH values compared to the I/R group. These results led us to conclude that BA may have beneficial effects on kidney tissue after testicular I/R.
BA did not significantly reverse GV and TCDN values compared to the I/R group. The reason why BA does not have a protective effect on some histological parameters may be due to the insufficient nephroprotective effect of BA. It is possible that this effect occurs in a dose-dependent manner. In a study conducted by Kar et al[42] by creating a renal ischemia reperfusion model in rats, in which higher dose of BA (i.p. application of 100 mg/kg) were administered, it was observed that the BA caused a decrease in glomerular damage, tubular damage, hyaline cast, and TD compared to the I/R group. The overall antioxidant support offered by BA may be insufficient in the face of the complex pathophysiology of kidney injury or may only be evident in very mild injury patterns. Also, as shown in animal studies, BA can cause direct damage to the kidney tubules and glomeruli at doses above the optimal preventive dose[56].
Another study in rats showed that renal I/R causes congestion, hemorrhage, hydropic degeneration, and tubular necrosis. In the experiment in which BA was administered intragastrically at a dose of 14 mg/kg 1 hour before ischemia, and combined with propolis, tubular necrosis and minimal degeneration of the tubular epithelium were observed in the combination group, with histological structures that were almost normal[49].
Biochemical markers of oxidative stress are more sensitive indicators of tissue damage and can be detected much earlier than histological changes[8]. MDA is one of the end products of the peroxidation of polyunsaturated fatty acids in cells. The increase in free radicals causes overproduction of MDA, and MDA level is generally known as a marker of oxidative stress[57]. In our study, MDA levels in kidney tissue increased in I/R-induced rats. Additionally, it was observed that MDA levels decreased after I/R in BA-administered subjects. The decrease in lipid peroxidation and MDA levels in rats that underwent I/R after BA administration was consistent with the results of similar studies in the literature[42,49]. Previous studies have shown that PON-1 expression is reduced by oxidative stress[58-60]. In our study, PON-1 enzyme activity was found to be significantly lower in the I/R group compared to the control and BA groups, in line with studies in the literature[23,30,61,62]. In addition, this value was found to be significantly higher in the BA-I/R group than in the I/R group. In a T/D experiment in rats conducted by Yesil et al[62], PON-1 enzyme activity in the I/R group was significantly lower than in the control group. Another experiment in rats fed a combination of BA and high-fat diet showed increased PON activity compared to the high-fat diet group[63].
In our study, the groups had similar GST and CAT enzyme activities. Although no significant difference was found between the groups, it was observed that these enzyme activities decreased in the I/R group, as in some similar studies in the literature[30,42]. In the BA-administered animals in the I/R group, a slight increase in CAT enzyme levels was observed compared to the I/R group, as in a similar study[42]. In a rat experiment in which malathion was administered and oxidative stress was induced, it was observed that BA administration reversed the malathion-induced changes in SOD and CAT activities in erythrocytes, liver, kidney, and brain tissue in a dose-dependent manner[64]. In the nephrotoxicity experiment induced by cisplatin toxicity conducted in rats by Hazman et al[48], a comparison of the data of the control group and the cisplatin group showed that BA applications lower than 200 mg/kg administered by gavage had no effect on CAT activity.
The lack of significant change in GST and CAT levels may be due to a biological equilibrium point. Consumption rates and production rates may have become equal. A review of time-dependent studies in the literature suggests that this phenomenon stems from the equilibrium phase between enzyme consumption and de novo synthesis in the acute phase.
The release of high amounts of ROS after I/R can rapidly deplete the available GST and CAT in the kidneys. But distant testicular I/R may be insufficient to significantly deplete these renal antioxidant reserves, unlike a direct renal I/R. The kidney have a strong defense mechanism within itself through the activation of other compensatory antioxidant pathways and can withstand mild systemic injuries without changing existing enzyme levels. The observed insufficient change may also be due to inadequate experimental design rather than a biological difference. The duration of ischemia applied to the testis may not be long or severe enough to trigger significant damage to the kidney. Also insufficient statistical power of the study may prevent a small effect (minimal enzyme change) from being considered statistically significant.
Longer ischemia and reperfusion times may show a greater impact on the kidneys. A review of studies in the literature reveals varying results regarding changes in antioxidant enzyme levels. In Vakili-Sadeghi et al’s study, 3 hours of torsion and 3 hours of detorsion were applied, and a decrease in GST was found in the testicular tissue[65]. In Cvetkovic et al’s study, 1 hour of torsion was applied, and on the 30th day, the CAT level in the plasma remained unchanged[8]. In a T/D experiment, after 2 hours of torsion and 2 hours of detorsion, a decrease in the antioxidant enzyme SOD and a decrease in total antioxidant status were observed in the lung tissue[28]. In another experiment in which 2 hours of testicular torsion and 4 hours of detorsion were applied, no significant changes were observed in kidney MDA, nitric oxide content and myeloperoxidase activity[29]. In another experiment in which 2 hours of ischemia and 2 hours of treatment were applied, GST, CAT and PON levels were found to be decreased in kidney and lung tissue[30].
I/R can occur in various situations in the human body. Examples include serious conditions, such as torsion (testicular, ovarian), major vascular surgery, organ transplantation, tourniquet use, compartment syndrome, and shock (hypovolemic, septic, etc.). The results obtained in this study can later be used to develop BA therapy for the treatment of I/R injuries that may occur in the human body in various ways.
In our study, we found that the T/D model we created in rat testis caused kidney damage and that BA application reduced specific aspects of the damage and oxidative stress in the kidneys to some extent. Among the parameters examined regarding the effect of BA, a decrease in TD and VVH damage scores, a decrease in MDA level, and an increase in PON-1 enzyme activity support our hypothesis. However, we think that the lack of significant changes in some histopathological parameters and GST and CAT enzyme activities and the fact that some results were different from some previous studies may be due to experimental conditions or methodology. Therefore, we believe that more accurate and enlightening results can be achieved by conducting such studies with larger samples and under similar conditions.
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