Chemoprotective effects of kolaviron on ethylene glycol monoethyl ether‐induced pituitary‐thyroid axis toxicity in male rats

Endocrine disrupting chemicals cause reproductive dysfunction by interacting with intricate regulation and cellular processes involve in spermatogenesis. This study investigated the probable mechanism of action of ethylene glycol monoethyl ether (EGEE) as an antiandrogenic compound as well as the effects of kolaviron upon co‐administration with EGEE in rats. Adult male rats were exposed to EGEE (200 mg kg^?1 bw) separately or in combination with either kolaviron [100 (KV1) and 200 (KV2) mg kg^?1 bw] or vitamin E (50 mg kg^?1 bw) for 14 days. Western blot analysis revealed that the administration of EGEE adversely affected steroidogenesis in experimental rats by decreasing the expression of steroid acute regulatory (StAR) protein and androgen‐binding protein (ABP). EGEE significantly decreased the activities of 3β‐hydroxysteroid dehydrogenase (3β‐HSD) and 17β‐hydroxysteroid dehydrogenase (17β‐HSD) but markedly increased sialic acid concentration in rat testes. EGEE‐treated rats showed significant decreases in plasma levels of luteinising hormone (31%), testosterone (57.1%), prolactin (80.9%), triiodothyronine (65.3%) and thyroxine (41.4%), whereas follicle‐stimulating hormone was significantly elevated by 76.9% compared to the control. However, co‐administration of kolaviron or vitamin E significantly reversed the EGEE‐induced steroidogenic dysfunction in rats. This study suggests that kolaviron may prove promising as a chemoprotective agent against endocrine pathology resulting from EGEE exposure.     

Cisplatin‐induced testicular dysfunction and its amelioration by Launaea taraxacifolia leaf extract

This study investigates the ameliorative potential of Launea taraxacifolia (LT) aqueous leaf extract on cisplatin‐induced testicular dysfunction in Wistar rats. Thirty rats were randomly divided into six groups (A–F) of 5 rats each: Group A which served as control received water; Group B was intraperitoneally (ip) injected 10 mg kg^?1 body wt cisplatin on day 21; Groups C and D were given 100 and 400 mg of LT via oral administration, respectively, for 21 days while Groups E and F received similar treatment as Groups C and D, respectively, and then exposed to ip administration of 10 mg kg^?1 body weight cisplatin on the 21st day. Exclusively, Cisplatin‐exposed Group B rats showed reduced sperm characteristics and increased sperm morphological abnormalities; distorted histological architecture of seminiferous tubules; significantly increased lipid peroxidation (LPO) and decreased activities of superoxide dismutase (SOD), catalase (CAT) and glutathione (GSH)levels in the testes. These parameters in LT alone treated Groups C and D were not markedly different compared with the control group. The rats with the combined treatment in Groups E and F showed significantly improved sperm parameters, testicular histo‐architecture and antioxidant enzymatic activities. Conclusively, aqueous extract of L. taraxacifolia has protective potential against cisplatin damage.     

Oral administration of Moringa oleifera oil but not coconut oil prevents mercury‐induced testicular toxicity in rats

This study was conducted to compare the effects of administration of coconut oil (CO) and Moringa oleifera oil (MO) on testicular oxidative stress, sperm quality and steroidogenesis parameters in rats treated with mercury chloride (HgCl₂). After 15 days of oral administration of CO (2 ml kg^?1 body weight) and MO (2 ml kg^?1 body weight) along with intraperitoneal (i.p.) administration of HgCl₂ (5 mg kg^?1 body weight) alone or in combination, we found that CO treatment did not protect against HgCl₂‐induced poor sperm quality (motility, count) as well as decreased testosterone level and 17β‐hydroxysteroid dehydrogenase (17β‐HSD) activity. Treatment with CO alone decreased glutathione (GSH), and glutathione peroxidase (GSH‐Px) activities and increased malondialdehyde (MDA) level in rat's testis, whereas MO did not change these parameters. Cotreatment with MO prevented HgCl₂‐induced testicular catalase (CAT) and superoxide dismutase (SOD) activities, poor sperm quality and low testosterone level and also blocks the adverse effect of CO+HgCl₂ (2 ml kg^?1 body weight + 5 mg kg^?1 body weight) on the investigated endpoints. In conclusion, MO and not CO decreased the deleterious effects of HgCl₂ on sperm quality and steroidogenesis in rats and also strengthen the antioxidant defence of the testes. Therefore, MO is beneficial as an antioxidant in HgCl₂‐induced oxidative damage.     

Gallic acid protects against cyclophosphamide‐induced toxicity in testis and epididymis of rats

The protective role of gallic acid (GA) on reproductive toxicity induced by cyclophosphamide (CPA), an antineoplastic drug, was investigated in male Wistar rats. Sixty rats were grouped into 10 rats per group. Group 1 (control) received distilled water. Rats in groups 2 and 3 received GA alone at 60 and 120 mg kg^?1 for 14 consecutive days, respectively. Group 4 received a single intraperitoneal dose of CPA at 200 mg kg^?1 on day 1. Groups 5 and 6 received a single dose of CPA (200 mg kg^?1) intraperitoneally on day 1 followed by treatment with GA at 60 and 120 mg kg^?1 for 14 consecutive days, respectively. In testes and epididymis of the treated rats, CPA administration resulted in significant elevation (P < 0.05) in malondialdehyde (MDA), nitrite and hydrogen peroxide levels. There was a significant decrease in the activities of superoxide dismutase and glutathione‐S‐transferase. Furthermore, there were significant reductions in plasma luteinising hormone (LH), follicle stimulation hormone (FSH) and testosterone levels, which were accompanied by significant decrease in sperm motility and viability in CPA‐treated rats. Histological examination revealed marked testicular and epididymal atrophy in CPA alone treated rats and these aberrations were reversed by GA. In conclusion, GA has capacity to protect against reproductive toxicity induced by cyclophosphamide.     

Dietary resistant maltodextrin ameliorates testicular function and spermatogenesis in streptozotocin–nicotinamide‐induced diabetic rats

This study investigated the effect of resistant maltodextrin (RMD) on reproduction in streptozotocin (STZ)–nicotinamide‐induced type 2 diabetic male rats. Forty male rats were induced with diabetes by a single intraperitoneal injection of STZ (50 mg kg^?1) and nicotinamide (100 mg kg^?1). Five groups were analysed in total: normal, diabetic rats without RMD, diabetic rats with RMD 1.2 g per 100 g diet (1×), with RMD 2.4 g per 100 g (2×), and with RMD 6.0 g per 100 g (5×). The groups of diabetic rats with the RMD supplement, compared to those without supplement, showed improved plasma glucose control, attenuated insulin resistance and recovery of testosterone level and spermatogenesis stage. The STZ–nicotinamide‐induced diabetes mellitus (DM) caused a significant reduction in serum testosterone, testis androgen receptor (AR), steroidogenic acute regulatory protein (StAR) and 3β‐hydroxysteroid dehydrogenase (3β‐HSD) protein, but a statistical recovery in each of these was observed in the 5× group. TUNEL‐positive cells were observed in the diabetic without RMD group, and RMD treatment reduced apoptotic germ cells. The expression of Bax/Bcl2 was induced in the diabetic group and also significantly reduced in the 5× group. Dietary RMD may improve metabolic control in STZ–nicotinamide‐induced diabetic rats and attenuate hyperglycaemia‐related impaired male reproduction and testicular function.     

Chemotherapeutic efficacy of an ethanolic Moringa oleifera leaf extract against chromium‐induced testicular toxicity in rats

This study was conducted to determine the mechanism underlying the chemotherapeutic efficacy of an ethanolic Moringa oleifera leaf extract (MOLEE) against chromium‐induced impairments of rat testes using biochemical methods. Twenty male Wistar rats were divided into four groups of five animals each. Group I (control), group II injected potassium dichromate (8 mg kg^?1) i.p., group III gastrogavaged MOLEE (500 mg kg^?1) p.o. and group IV received (potassium dichromate plus MOLEE) by the same doses for 60 days. After the blood samples were collected, the animals were sacrificed to determine the testicular antioxidant status and sperm parameters. The chromium‐treated group exhibited a significant decrease in testicular antioxidant enzymatic activities, local immunity and sperm parameters as well as an increase in inflammatory markers when compared with the control and MOLEE‐treated group. However, concurrent administration of chromium and MOLEE significantly ameliorated the chromium effects on the sperm parameters, local immunity, inflammatory markers and antioxidant enzymatic activities compared with rats exposed to chromium alone. This study concludes that chronic exposure to chromium produces clear testicular toxicity, which can either be prevented or at least decreased by concomitant administration of MOLEE. Interestingly, the metal ion chelation could attribute partly the antioxidant activities of MOLEE.     

Quercetin prevents docetaxel‐induced testicular damage in rats

The protective effect of quercetin on docetaxel – an anticancer agent – induced testicular damage in rats was investigated. Thirty‐two rats were randomly divided into four groups: group 1 – control, carrier solutions were given; group 2 – quarcetin 20 mg kg^?1 day^?1 was given orally; group 3 – docetaxel 5 mg kg^?1 was given intraperitoneally as single dose; group 4 – docetaxel and quarcetin were given together. The histopathological changes; the specific biochemical markers, including antioxidants; and the sperm characteristics were evaluated. Docetaxel caused a significant increase in TBARS level and a significant decrease in SOD, GPX, CAT and GSH levels in the testicular tissues compared with the control group, whereas quercetin led to a significant decrease in lipid peroxidation, which was caused by docetaxel, via reducing TBARS level and increasing the levels of SOD, CAT, GPX and GSH. In addition, after docetaxel administration, sperm motility, sperm concentration, testicular and epididymis weights were significantly decreased and abnormal sperm rate and histopathological changes were increased. However, these effects of docetaxel on sperm parameters, histological changes and the tissue weights were eliminated by quercetin treatment. Our results show that the administration of docetaxel induced the testicular damage (oxidative stress, testes tissue damage and sperm parameters), and quercetin prevented docetaxel‐induced testicular damage in rats.     

3,3 diindolylmethane leads to apoptosis,decreases sperm quality,affects blood estradiol 17 β and testosterone,oestrogen (α and β) and androgen receptor levels in the reproductive system in male rats

3,3 Diindolylmethane (DIM) is a major digestive product of indole‐3 carbinol, obtained from Brassica family vegetables such as broccoli, cabbage and Brussels sprouts. This study aimed to investigate the effects of DIM on sperm parameters, histological structures of testicular tissues, blood testosterone (T) and estradiol 17‐β (E2) in male rats. Thirty‐eight male Sprague Dawley rats were used. Rats were divided into four groups: Group I: referred as Control group, received corn oil only; Group II: as DIM‐10, rats received 10 mg kg^?1 DIM; Group III: as DIM‐50, rats received 50 mg kg^?1 DIM; Group IV: as DIM‐100, received 100 mg kg^?1 DIM during 53 days. Spermatological parameters, malondialdehyde (MDA) levels of testes and serum T and E2 levels were assayed. Histopathological examinations of tests were done. DIM caused an increase in MDA levels. It decreased motility and live sperm rates and increased degeneration of testicular tissues. While DIM‐10 did not affect abnormal sperm rate, higher concentrations increased the abnormalities. Sperm density was higher in DIM‐10 groups when compared to both other groups. Only DIM‐50 had an anti‐androgenic effect among all groups. Only, DIM‐10 showed anti‐estrogenic activity as compared to higher DIM groups. In conclusion, DIM (i) had side effect on some sperm characteristics, (ii) increased the MDA levels and (iii) led to histological degeneration of testicular tissues and apoptosis in a dose‐dependent manner.     

Antioxidant enzymes activity,lipid peroxidation,oxidative damage in the testis and epididymis,and steroidogenesis in rats after co‐exposure to atrazine and ethanol

Concomitant alcohol use and exposure to xenobiotics can adversely affect gonadal functions. This study investigated the oxidative status of the testis and epididymis and steroidogenesis of rats co‐exposed to ethanol (EtoH, 5 mg kg^?1 b.wt.) and atrazine (ATZ, 50, 100, 300 mg kg^?1 b.wt.) for 3 weeks. The activities of catalase, superoxide dismutase, glutathione peroxidase, as well as the concentrations of glutathione and malondialdehyde, as indicators of oxidative stress were measured in the homogenates of the testis and epididymis. Testosterone and cholesterol concentrations as well as 17β‐hydroxysteroid dehydrogenase (17β‐HSD) activity were assayed in the plasma and testis respectively. After the administration of EtoH alone, or in combination with different doses of ATZ, oxidative damage as evident by malondialdehyde level was not observed in both the testis and epididymis. The combine exposure group showed dose‐dependent decrease in plasma testosterone and testis cholesterol level and increase in testis 17β‐HSD activity compared to the EtoH group. Furthermore, the testes and epididymis of the EtoH‐exposed rats treated with high dose of ATZ had severe histopathological damage. Therefore, ATZ‐exposed alcohol‐treated rats have histological damage of the testis and epididymis and lower testosterone level than EtoH‐treated rats.     

Rutin ameliorates cisplatin‐induced reproductive damage via suppression of oxidative stress and apoptosis in adult male rats

Cisplatin (CP) treatment causes damage in the male reproductive system. Rutin (RUT) is a naturally occurring flavonoid glycoside that has antioxidant and anti‐inflammatory properties. This study aimed to investigate effects of RUT against cisplatin‐induced reproductive toxicity in male rats. Twenty‐one adult male Sprague Dawley rats were used. The control group received physiological saline with oral gavage during 14 days, and physiological saline was injected intraperitoneally (IP) in 10th days of study. CP Group received physiological saline during 14 days, and 10 mg kg^?1 CP was injected IP in 10th day. RUT + CP group received RUT (150 mg kg^?1) during 14 days, and 10 mg kg^?1 CP was injected IP in 10th day. Spermatological parameters (including motility, cauda epididymal sperm density, dead sperm percentage and morphological sperm abnormalities), biochemical (MDA, GSH, GSH‐px, SOD and CAT), histological (H&E dye) and immunochemistry evaluations of testicles were evaluated. CP treatment caused damage on some spermatological parameters, increased the oxidative stress and induced testicular degeneration and apoptosis when compared to the control group. However, RUT treatment mitigates these side effects when compared to the CP alone group. IT is concluded that RUT treatment may reduce CP‐induced reproductive toxicity as a potential antioxidant compound.     

Quercetin ameliorates polychlorinated biphenyls‐induced testicular DNA damage in rats

Polychlorinated biphenyls (PCBs) are a group of environmental contaminants widely reported to cause gonadal toxicity in both humans and animals. This study investigated the amelioratory role of quercetin in PCBs‐induced DNA damage in male Wistar rats. Polychlorinated biphenyls were administered intraperitoneally at a dose of 2 mg kg^?1 alone or in combination with quercetin (orally) at 50 mg kg^?1 for 25 days. Quercetin modulation of PCBs‐induced gonadal toxicity was evaluated using selected oxidative stress indices, comet assay, measurement of DNA concentration and histology of the testes. Administration of PCBs alone caused a significant (P < 0.05) depletion in the total thiol level in testes of treated rats. Conversely, the levels of reactive oxygen species (ROS) and thiobarbituric acid reactive substances (TBARS) production were markedly elevated in testes of PCBs‐treated rats compared with control. Further, PCBs exposure produced statistically significant increases in DNA tail migration, degraded double‐stranded DNA (dsDNA) concentration and histological alterations of testes of the treated rats compared to control. Quercetin cotreatment significantly improved the testicular antioxidant status, decreased DNA fragmentation and restored the testicular histology, thus demonstrating the protective effect of quercetin in PCBs‐treated rats.     

Quercetin exacerbates the effects of subacute treatment of atrazine on reproductive tissue antioxidant defence system,lipid peroxidation and sperm quality in rats

The study investigated the reproductive function and the antioxidant defence system of rats co‐exposed to atrazine [ATZ, 120 mg kg^?1 body weight (b. wt)] and quercetin (QT, 20 mg kg^?1 b. wt.). ATZ had no significant effects on feed intake, body weights and reproductive organs weight except prostate weight. Sperm abnormalities were increased, whereas sperm production, sperm motility and epididymal and testicular sperm numbers were decreased with ATZ treatment. Antioxidant enzymes including superoxide dismutase, glutathione‐S‐transferase and glutathione peroxidase were significantly altered in the epididymis and testis resulting to lipid peroxidation. A potentiating response on glutathione‐S‐transferase and aspartate aminotransferase activities in the testis and on lactate dehydrogenase activity and glutathione level in the epididymis was observed in the QT + ATZ animals. Quercetin alone decreased seminal vesicle and prostate weights, increased superoxide dismutase activity in the testis and ascorbate level in the epididymis. Mild pathological changes were observed in the ATZ group, whereas considerable necrosis of seminiferous tubular cells with hypoplasia of the epithelia was observed in the QT + ATZ animals. The epididymis of these animals had multilayered and sometimes a single lining epididymal epithelium with few spermatozoa. We conclude that quercetin at the investigated dose increases the susceptibility of rat reproductive tissues to atrazine‐induced oxidative damage.     

Fenugreek seed extract attenuates cisplatin‐induced testicular damage in Wistar rats

Cisplatin (CIS) provides oxidative stress and inflammations in testicular tissues. Fenugreek seed extract (FSE) is a widely used herbal medicine with potent antioxidant and anti‐inflammation properties. The purpose of this study was to investigate the protective effects and the possible mechanisms of FSE against CIS‐induced testicular damage in rats. Adult male Wistar rats were given vehicle, single dose of CIS alone (10 mg kg^?1), single dose of FSE alone or single dose of CIS followed by FSE (50, 100 or 200 mg kg^?1) every day for 5 days. On day 6, oxidative stress and apoptotic testicular toxicity were evaluated. FSE attenuated both germ cell degenerations and apoptosis in seminiferous tubules in CIS‐treated rats. Furthermore, FSE counteracted CIS‐induced oxidative stress in rats as assessed by the restoration of superoxide dismutase and catalase activities and reduction in the myeloperoxidase activity and malondialdehyde levels in testes. CIS increased expressions of inducible nitric oxide synthase and nuclear factor‐kappa B in testicular tissues. Importantly, treatment with FSE at all doses effectively alleviated all of these inflammatory parameters in testes. Based on these results, we concluded that FSE reduces CIS‐induced reproductive toxicity in rats by the suppression of testicular oxidative stress, apoptosis and inflammations.     

Protective effects of udenafil citrate,piracetam and dexmedetomidine treatment on testicular torsion/detorsion‐induced ischaemia/reperfusion injury in rats

The aim of this study was to investigate the antioxidant properties of udenafil citrate (1.4 mg kg^?1–2.8 mg kg^?1), dexmedetomidine 25 μg kg^?1 and piracetam 200 mg kg^?1 administered on ipsilateral/contralateral testes after ischaemia in a rat model of testicular torsion/detorsion (T/D) and define its protective effect histologically. Fifty‐six Wistar albino rats were included and randomly assigned into 6 groups. No intervention was performed in control group (Group 1, n = 8) and in torsion/detorsion group, (Group 2, n = 8). Udenafil 1.4 mg kg^?1 was given to torsion/detorsion group (Group 3, n = 10), udenafil 2.8 mg kg^?1 was given to torsion/detorsion group (Group 4, n = 10), piracetam 200 mg kg^?1 was given to torsion/detorsion group (Group 5, n = 10) and dexmedetomidine 25 μg kg^?1 was given to torsion/detorsion group (Group 6, n = 10) intraperitoneally after 60 mins of testicular torsion. Biochemical and histopathological testicular injury were evaluated. When the tissue was examined by TOS values, Group 3, Group 4 and Group 5 were significantly lower than Group 2. In contrary Group 6 values were significantly higher than Group 2. The increasing doses of udenafil demonstrated antioxidant properties on the testis tissue and histopathological that protects the testicles.     

Thymoquinone therapy abrogates toxic effect of cadmium on rat testes

The protective effect of thymoquinone was investigated against cadmium‐induced testicular toxicity in rats. Testicular toxicity was induced by a single intraperitoneal (i.p.) injection of cadmium chloride (2 mg kg^?1). Thymoquinone treatment (10 mg kg^?1 day^?1, i.p.) was applied for five consecutive days, starting 3 days before cadmium administration. Thymoquinone significantly attenuated the cadmium‐induced decreases in serum testosterone, and testicular reduced glutathione and superoxide dismutase activity and significantly decreased the elevations of testicular malondialdehyde, nitric oxide and cadmium ion levels resulted from cadmium chloride administration. Also, thymoquinone ameliorated the cadmium‐induced testicular tissue injury observed by histopathological examination. In addition, thymoquinone significantly decreased the cadmium‐induced expression of inducible nitric oxide synthase, tumour necrosis factor‐α, cyclooxygenase‐2, nuclear factor‐κB and caspase‐3 in testicular tissue. It was concluded that thymoquinone, through its antioxidant and anti‐inflammatory activities, may represent a potential candidate to protect the testes against the detrimental effect of cadmium exposure.     

Dose‐dependent effects of ethanol extract of Salvia haematodes Wall roots on reproductive function and copulatory behaviour in male rats

This study was aimed to investigate the dose‐dependent effects of Salvia haematodes Wall roots (SHW) extract on male reproductive function and copulatory behaviour in rats. Sexually mature males were assigned to four groups: control and treated (5, 50 and 300 mg kg^?1 day^?1 for 30 days). At the end of treatment regimes, the reproductive activity viz. body/organ weights, testicular spermatogenesis, daily sperm production rate (DSP) and epididymal sperm counts, and sexual behaviour including mounting latency (ML), mounting frequency (MF), intromission latency (IL), intromission frequency (IF), ejaculation latency (EL), post‐ejaculatory interval (PEI) and penile reflexes (PE) were assessed. Results showed significant increase in body weight (at 300 mg kg^?1), testis/epididymis weights (at 50 and 300 mg kg^?1), testicular spermatids, DSP, tubular diameter and epididymal sperm counts (at 50 and 300 mg kg^?1doses) in treated compared with control rats. It also produced dose‐dependant changes in sexual behaviour. The 5 mg kg^?1 dose of extract increased MF and PE, whereas 50 and 300 kg^?1 doses caused significant increase in MF, IF, PE, EL (but less than sildenafil citrate treatment), hit rate and seminal plug weight. It is concluded that SHW extract enhances anabolic activity, testicular function and sexual behavioural performance in a dose‐dependant manner.     

Effects of montelukast and zileuton on testicular torsion/detorsion injury in rats

The aim of this study was to evaluate and compare the effects of 5‐lipoxygenase enzyme (5‐LO) inhibitor zileuton and cysteinyl leukotriene receptor (CysLT1R) antagonist montelukast in testicular torsion/detorsion (T/D) injury model in rats. Rats were anaesthetised with 75 mg kg^?1 ketamine hydrochloride and 8 mg kg^?1 xylazine intraperitoneal before the operation. Torsion was created by rotating the right testis 720° clockwise and maintained by fixing the testis. The rats were treated with CysLT1R antagonist montelukast (10 mg kg^?1; i.p.), 5‐LO inhibitor zileuton (3 mg kg^?1; i.p.), and vehicle, at 30 min prior detorsion. After 1 h of torsion, the testis was counter‐rotated to the natural position and replaced into the scrotum. Malondialdehyde (MDA) level was measured in testicular tissue after 3 h of reperfusion. Histological examination was performed after 24 h of reperfusion. T/D caused a significant increase in MDA level and histopathological injury in testes. Montelukast and zileuton treatments prevented the T/D‐induced augmentation in MDA levels. Only zileuton treatment significantly reduced the T/D‐induced histopathological injury. In this study, we demonstrated for the first time that zileuton had protective effects on testicular T/D injury. We have also found that zileuton is more effective than montelukast on histopathological injury.     

Bioefficacy of hydromethanolic extract of tuber of Chlorophytum borivilianum (Safed Musli) for the management of male infertility in cyproterone acetate‐treated albino rats

Increase in male sexual dysfunction, and its treatment with conventional aphrodisiac drugs with side effects lead to investigate the spermatogenesis and androgenesis augmentative efficacy of hydromethanolic (40 : 60) extract of root of Chlorophytum borivilianum (family – Liliaceae) against cyproterone acetate‐induced subfertility in Wistar strain male albino rat. For this purpose, experimental rats were divided into three treatment groups: vehicle (received distilled water), cyproterone acetate (gastric intubation at 250 mg kg^?1 twice daily for 35 days) and cyproterone acetate plus root extract of C. borivilianum (gastric intubation at 250 mg kg^?1 plus 400 mg kg^?1 with an interval of 20 min twice daily for 35 days). After 35‐day treatment, all rats were euthanised. Reproductive deviations towards negative side were investigated by screening the spermatogenic and steroidogenic biosensors. Oxidative stress profile in reproductive organs and sperm pellet was evaluated by biochemical assessment of antioxidative enzyme activities and level of end products of the lipid peroxidation. Apoptosis profile was evaluated by Western blot study, TUNEL assay and DNA fragmentation study of testicular tissues. Evaluation of toxicity profile was included for experimental investigation. After cyproterone acetate treatment, the pituitary–testicular axis was deviated towards the negative side and its tuning system was affected by oxidative stress and apoptosis‐mediated process, which reduced the quality of semen and finally led to subfertility. Co‐administration of C. borivilianum root extract enhanced male reproductive potentiality and prevented the negative deviations after the treatment with cyproterone acetate by means of increasing oxidative defence and maintaining homeostasis in testicular apoptosis process.     

Ameliorative effect of polydatin on oxidative stress‐mediated testicular damage by chronic arsenic exposure in rats

Arsenic causes lipid peroxidation leading to alterations in antioxidant status in organisms. In this study, the reproductive effects of chronic exposure to arsenic and the protective effects of polydatin (PD) were evaluated in 35 Wistar male rats, which were divided equally into five groups. The control group received a normal diet and tap water, arsenic (100 mg l^?1, approximately 1/50 of oral LD₅₀) was given via drinking water to experimental groups except control group, and PD was orally given to the other groups at dose of 50, 100 and 200 mg kg^?1 for 60 days. Arsenic administration decreased sperm motility, glutathione level, superoxide dismutase and catalase activities in testicular tissue of rats. In contrast, malondialdehyde level and DNA damage were found to be high levels in arsenic‐treated group. Histopathologically, it was observed that decreased sperm concentration and degeneration of Sertoli cells in testicular tissue. PD administration, partially 200 mg kg^?1, reversed arsenic‐induced lipid peroxidation, DNA damage, antioxidant enzyme activity and cell integrity in testis of rats. These results demonstrate that PD decreases arsenic‐induced lipid peroxidation, enhances the antioxidant defence mechanism and regenerates tissue damage in testis of rats.     

Protective effects of quercetin against arsenic‐induced testicular damage in rats

This study investigated the effect of quercetin on changes in testes due to arsenic exposure. Twenty‐seven male rats were divided into three groups: control (10 ml kg^?1 day^?1 saline), arsenic (10 mg kg^?1 day^?1 sodium arsenite) and arsenic + quercetin (arsenic + 50 mg kg^?1 day^?1 quercetin). The rats were sacrificed at the end of 15‐day experiment. There was no difference between control group and arsenic group in body weight gain, testicular weight and serum total testosterone level. Quercetin treatment did not cause a significant difference in these parameters. In the arsenic group rats, we determined deterioration in the structure of seminiferous tubules, a decrease in the number of spermatogenic cells, an increase in the number of apoptotic cells, a decrease in the number of PCNA‐positive cells, a decrease in SOD, CAT and GSH‐Px activities, and an increase in the MDA level in testicular tissue. In all these changes, arsenic+quercetin group showed an improved compared to arsenic group. The amount of arsenic increased in the arsenic group was compared to the control group, and there was no difference between arsenic group and arsenic + quercetin group in the amount of arsenic. In conclusion, quercetin prevented arsenic‐induced testicular damage with its anti‐apoptotic and antioxidant effects.