Protective effects of Fumaria parviflora L. on lead‐induced testicular toxicity in male rats

In recent years, the clinical importance of herbal drugs has received considerable attention in reducing free radical‐induced tissue injury. Oxidative stress has been proposed as a possible mechanism involved in lead toxicity that causes reproductive system failure in both human and animals. Fumaria parviflora L., a traditional herb, has been used to cure various ailments in Persian folk medicine. This study was carried out to investigate whether ethanolic extract of F. parviflora leaves could protect the male rats against lead‐induced testicular oxidative stress. Adult Wistar rats were treated with 0.1% lead acetate in drinking water with or without 200 mg kg day^?1 F. parviflora extract via gavage for 70 days. Lead acetate treatment resulted in significant reduction in testis weight, seminiferous tubules diameter, epididymal sperm count, serum testosterone level, testicular content of superoxide dismutase (SOD) and glutathione peroxidase (GPx). Moreover, significant elevation was observed in content of malondialdehyde (MDA) in lead‐treated rats. However, co‐administration of F. parviflora extract showed a significant increase in selected reproductive parameters in lead‐treated rats. The results indicated that ethanolic extract of F. parviflora leaves has a potential to restore the suppressed reproduction associated with lead exposure and prevented lead‐induced testicular toxicity in male Wistar rats.     

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.     

Combined effects of chronic hyperglycaemia and oral aluminium intoxication on testicular tissue and some male reproductive parameters in Wistar rats

Exposure to either environmental toxicants or chronic hyperglycaemia could impair male reproductive function. However, the extent to which exposure to such toxicants, in the presence of pre‐existing metabolic dysfunction, could affect male reproduction is unclear. Streptozotocin‐induced diabetic Wistar rats (12 weeks old) were exposed to oral aluminium chloride at 250 ppm for 30 days; followed by evaluation of caudal epididymal sperm count and motility, assay for serum follicle stimulating hormone (FSH), testosterone (T) and oestradiol; and assessment of testicular histology. Moreover, blood glucose was evaluated by the glucose oxidase method. In rats treated with streptozotocin (STZ) or aluminium (Al) alone, erosion of testicular parenchyma and stroma was observed. This effect was most severe in diabetic rats simultaneously exposed to Al; coupled with reduced caudal epididymal sperm count that was least in this (STZ+Al) group (18.75 × 10⁶ ml^?1) compared with controls (61.25 × 10⁶ ml^?1; P < 0.05), STZ group or Al group. Moreover, these reproductive perturbations (in the STZ+Al group) were associated with reduced sperm motility and significantly reduced serum FSH (P < 0.05); but elevated serum T and oestradiol (P < 0.05), compared with control. These suggest that diabetes‐induced testicular lesion is exacerbated by simultaneous oral Al toxicity in Wistar rats.     

Aqueous fruit extract of Mimusops elengi causes reversible suppression of spermatogenesis and fertility in male mice

Antifertility efficacy of oral administration of aqueous fruit extract of Mimusops elengi (200, 400 and 600 mg kg^?1 body weight/day for 35 days) was evaluated in Parkes strain male mice. Various reproductive end points such as histopathology, sperm parameters, testosterone level, haematology, serum biochemistry and fertility indices were assessed; activities of 3β‐ and 17β‐hydroxysteroid dehydrogenases, and immunoblot expressions of StAR and P450scc in the testis were also assessed. Histologically, testes in Mimusops‐treated mice showed nonuniform and diverse degenerative changes in the seminiferous tubules; both affected and normal tubules were observed in the same sections of testis. The treatment had adverse effects on testicular hydroxysteroid dehydrogenases and StAR and P450scc, serum level of testosterone and on motility, viability and number of spermatozoa in cauda epididymis. However, serum levels of alanine aminotransferase, aspartate aminotransferase and creatinine, and haematological parameters were not affected by the treatment. Also, libido was not affected in treated males, but their fertility was markedly suppressed. By 56 days of treatment withdrawal, the alterations caused in the above parameters recovered to control levels, suggesting that Mimusops treatment causes reversible suppression of spermatogenesis and fertility in Parkes mice. Further, there were no detectable signs of toxicity in treated males.     

Strontium fructose 1, 6‐diphosphate alleviate cyclophosphamide‐induced oligozoospermia by improving antioxidant and inhibiting testicular apoptosis via FAS/FASL pathway

This study investigated the treatment effects of a new compound, strontium fructose 1, 6‐diphosphate (FDP‐Sr), in cyclophosphamide (CP)‐induced oligozoospermia. FDP‐Sr, with extra high‐energy supply, could reverse male hypogonadism in the testis. Male Wistar rats were randomly divided into three groups: control group (vehicle treated), CP group and CP + FDP‐Sr group. Both CP group and CP + FDP‐Sr groups were orally administered CP (20 mg kg^?1) consecutively for the first 7 days to establish CP‐induced testicular toxic models. Subsequently, CP group was given orally distilled water per day, whereas CP + FDP‐Sr group was received FDP‐Sr (200 mg kg^?1) for 49 days. Compared to the CP group, the FDP‐Sr group showed significantly increased levels of serum testosterone, testis relative weights and epididymal sperm counts in rats. In addition, rats treated by FDP‐Sr showed the recuperative activities of testicular marker enzymes and normalised levels of antioxidants in tissue. Testicular protection of FDP‐Sr was further demonstrated by enhancing expression of P450scc, reducing ability of FAS/FASL and generating cytoprotection in the histopathological study. FDP‐Sr appeared to possess an ability to attenuate CP‐induced reproduction toxicity via the activation of antioxidants and steroidogenesis enzymes, and alleviate oligozoospermia via inhibition of testicular apoptosis by FAS/FASL pathway.     

Effect of rutin on diabetic‐induced erectile dysfunction: Possible involvement of testicular biomarkers in male rats

The present study aimed to investigate effects of rutin on diabetic‐induced impairments of sexual behaviour, spermatogenesis and oxidative testicular damage. Diabetes was induced by a single injection of STZ (65 mg/kg) in male adult Wistar rats. Two weeks later, rutin (50 and 100 mg kg^?1 day^?1) was treated to normal and diabetic rats for 5 weeks. Sexual behaviour of the animals was observed by taking stimulus females. At the end of the study, sperm count, motility and viability were recorded. Serum levels of glucose, inflammatory markers and testosterone were also estimated. In penile tissue, cGMP levels were measured, while lipid peroxidation and antioxidant molecules and enzyme activities were determined. Finally, histopathological changes were evaluated in a cross‐section of testis. Diabetic‐induced alterations in male sexual behaviour and sperm count, motility and viability were markedly corrected following 5 weeks of rutin treatment to the diabetic animals. Rutin also attenuated the inhibited serum testosterone and penile cGMP content, while improved diabetic‐associated inflammation and testicular lipid peroxidation and oxidative stress. Histopathological evaluation revealed damaged testicular tissues in diabetic rats, which was protected following rutin treatment. In conclusion, treatment with rutin improved sexual functionality and also protects against diabetic‐induced testicular damage.     

Therapeutic effect of pentoxifylline on reproductive parameters in diabetic male mice

In this study, we aimed to investigate the effects of pentoxifylline (PTX) on male reproductive parameters in diabetic mice. Male adult mice (n = 24) were divided into control and three experimental groups (n = 6) including Diabetic, Diabetic + PTX and PTX groups. Diabetes was induced by single injection of streptozotocin (60 mg kg^?1). PTX was administered intraperitoneally at the dose of 12 mg kg^?1 for 14 days 1 week after diabetes induction. Serum levels of testosterone and blood glucose were determined and collected spermatozoa from cauda epididymidis analysed. Based on histological slides prepared from testis, the diameter of seminiferous tubules was determined using Motic camera and software and also apoptosis using TUNEL assay. Data were analysed using one‐way anova method, and P < 0.05 was considered statistically significant. The mean of seminiferous tubules diameter, final body weight, testis weight, sperm parameters and testosterone hormone level in PTX‐treated diabetic group indicated a significant increase compared to diabetic one, whereas apoptosis index and blood glucose were decreased in this comparison (P < 0.05). These results suggest that intraperitoneal administration of PTX is a potentially beneficial agent to reduce testicular damage and improves sperm parameters in diabetic mice by decreasing the ratio of apoptosis.     

Adverse effects of leptin on histone‐to‐protamine transition during spermatogenesis are prevented by melatonin in Sprague‐Dawley rats

This study examines the effect of melatonin on leptin‐induced changes in transition of histone to protamine in adult rats during spermatogenesis. Twelve‐week‐old Sprague‐Dawley rats were randomised into control, leptin‐, leptin–melatonin‐10‐, leptin–melatonin‐20‐ and melatonin‐10‐treated groups with six rats per group. Leptin was given via intraperitoneal injections (i.p.) daily for 42 days (60 μg/kg body weight). Rats in the leptin‐ and melatonin‐treated groups were given either 10 or 20 mg day^?1 kg^?1 body weight of leptin in drinking water. Melatonin‐10‐treated group received only 10 mg of melatonin day^?1 kg^?1 body weight in drinking water for 42 days. Control rats received 0.1 ml of 0.9% saline. Upon completion of the treatment, sperm count, morphology and histone‐to‐protamine ratio were estimated. Gene expression of HAT, HDAC1, HDAC2, H2B, H2A, H1, PRM1, PRM2, TNP1 and TNP2 was determined. Data were analysed using ANOVA. Sperm count was significantly lower, whereas the fraction of spermatozoa with abnormal morphology, the ratio of histone‐to‐protamine transition and the expressions of HAT, HDAC1, HDAC2, H2B, H2A, H1, PRM1 were significantly higher in leptin‐treated rats than those in controls or melatonin‐treated rats. It appears that exogenous leptin administration adversely affects histone‐to‐protamine transition, which is prevented by concurrent administration of melatonin.     

Preventive effect of Pueraria mirifica on testosterone‐induced prostatic hyperplasia in Sprague Dawley rats

Pueraria mirifica (PM) extract contains phytoestrogen daidzein and genistein. In this study, we investigated the protective effect of PM extract, daidzein and genistein on a testosterone‐induced prostatic hyperplasia in rats. Testosterone was administered at 3 mg kg^?1 to rats followed by the PM extract, daidzein and genistein for a period of 30 days with finasteride as positive control. The testosterone level was increased, indicating inhibition of 5α‐reductase converting testosterone to dihydrotestosterone. This was confirmed by prostate‐specific antigen level that significantly decreased when treated with PM extract, daidzein and genistein. The PM extract, daidzein and genistein reduced the increase in the prostate/body weight ratio in testosterone‐induced rats. This gives indication that PM extract, daidzein and genistein possessed protective activity for the treatment of benign prostatic hyperplasia. The analysis of histoarchitechture of the prostate has also shown that there was a significant improvement in prostatic cells of the testosterone‐induced rats when treated with PM extract, daidzein and genistein.     

Effects of leptin on sperm count and morphology in Sprague‐Dawley rats and their reversibility following a 6‐week recovery period

Altered epididymal sperm count and morphology following leptin treatment has been reported recently. This study examined the effects of 42 days of leptin treatment on sperm count and morphology and their reversibility during a subsequent 56‐day recovery period. Twelve‐week‐old male Sprague‐Dawley rats were randomised into four leptin and four saline‐treated control groups (n = 6). Intraperitoneal injections of leptin were given daily (60 μg Kg^?1 body weight) for 42 days. Controls received 0.1 ml of 0.9% saline. Leptin‐treated animals and their respective age‐matched controls were euthanised on either day 1, 21, 42 or 56 of recovery for collection of epididymal spermatozoa. Sperm concentration was determined using a Makler counting chamber. Spermatozoa were analysed for 8‐hydroxy‐2‐deoxyguanosine and DNA fragmentation (Comet assay). Data were analysed using anova . Sperm concentration was significantly lower but fraction of abnormal spermatozoa, and levels of 8‐hydroxy‐2‐deoxyguanosine were significantly higher in leptin‐treated rats on day 1 of recovery. Comet assays revealed significant DNA fragmentation in leptin‐treated rats. These differences were reduced by day 56 of recovery. It appears that 42 days of leptin treatment to Sprague‐Dawley rats has significant adverse effects on sperm count and morphology that reverse following discontinuation of leptin treatment.     

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.     

Antioxidant effect of manganese on the testis structure and sperm parameters of formalin‐treated mice

Manganese inhibits oxidative stress damage. The aim of this study was to investigate the protective role of manganese on testis structure and sperm parameters in adult mice exposed to formaldehyde (FA). Twenty adult male NMRI mice were selected and randomly divided into four groups: (i) control; (ii) sham; (iii) ‘FA’‐exposed group; and (iv) ‘FA and manganese chloride’‐exposed group. The FA‐exposed groups received 10 mg kg^?1 FA daily for 14 days, and manganese chloride was just injected intraperitoneally 5 mg kg^?1 on 2nd weeks. Mice were sacrificed, and spermatozoa were collected from the cauda of the right epididymis and analysed for count, motility, morphology and viability. The other testicular tissues were weighed and prepared for histological examination upon removal. Seminiferous tubules, lumen diameters and epithelium thickness were also measured. The findings revealed that FA significantly reduced the testicular weight, sperm count, motility, viability and normal morphology compared with control group (P ≤ 0.05). In addition, seminiferous tubules atrophied and seminiferous epithelial cells disintegrated in the FA group in comparison with the control group (P ≤ 0.05). However, manganese improved the testicular structure and sperm parameters in FA‐treated mice testes (P ≤ 0.05). According to the results, manganese may improve and protect mice epididymal sperm parameters and testis structure treated with FA respectively.     

Attenuation of the cyproterone acetate‐induced testicular hypofunction by a novel nutraceutical lycopene: a genomic approach

This study was designed to explore the cyproterone acetate (CPA)‐induced andrological hypofunction and its correction by oral administration of lycopene. In this concern, spermatogenic, biochemical, histological and genomic profiles were studied. Cyproterone acetate administration for 1 month helped to develop infertile model rats. A significant recovery was noted in sperm motility, sperm count, sperm viability, hypo‐osmotic swelling tail‐coiled spermatozoa; activities of testicular ?⁵, 3β‐hydroxysteroid dehydrogenase (HSD), 17β‐HSD, catalase (CAT) and superoxide dismutase (SOD); and levels of conjugated diene (CD), malondialdehyde (MDA), testicular cholesterol and serum testosterone after the administration of lycopene at 1.5 mg/0.5 ml Tween‐80/100 g body weight/day for last 1 month to infertile model rats. Simultaneously, qRT‐PCR study of Bax, Bcl‐2, caspase‐3, ?⁵, 3β‐HSD and 17β‐HSD genes in testicular tissue showed a significant rectification towards the control in CPA‐pre‐treated cum CPA–lycopene‐cotreated rats. Side‐by‐side histological and histometric studies showed a significant correction in qualitative analysis of spermatogenesis and seminiferous tubular diameter (STD) in CPA‐pre‐treated cum CPA–lycopene‐cotreated rats. Lycopene showed outstanding efficacy in the management of CPA‐induced testicular hypofunction with special reference to correction in oxidative stress‐induced testicular apoptosis at genomic level.     

Terazosin‐induced alterations in catalase expression and lipid peroxidation in the rat seminal vesicles

Previous studies have shown that alpha1‐adrenergic receptor antagonists may alter seminal vesicle contractility and impair fertility in male rats. This study was designed to investigate the effects of terazosin on the catalase expression in the seminal vesicles and the lipid peroxidation of the seminal fluid in normal adult rats. Wistar rats were treated with terazosin (1.2 mg kg^?1 body weight, given orally every second day) for 120 days. Catalase expression was assessed immunohistochemically in tissue sections of the seminal vesicles, and lipid peroxidation was estimated by measuring the malondialdehyde (MDA) levels in the seminal vesicles' fluid. The seminal vesicles in terazosin‐treated rats were particularly distended in comparison with those of controls, and their secreting epithelium was suppressed. Cytoplasmic catalase expression in the secreting epithelial cells (% of cells) was increased in terazosin‐treated specimens in comparison with controls (76.1 ± 17.1 versus 51.3 ± 25.1, P = 0.005). MDA levels (μm ) were also higher in samples from treated subjects in comparison with controls (2.67 ± 1.19 versus 1.39 ± 0.19, P = 0.01). Although the direct effect of terazosin treatment on the seminal vesicles is that of impaired contractility, an indirect effect is that on fertility by increasing lipid peroxidation in the seminal fluid and/or through degrading of hydrogen peroxide that is essential for sperm capacitation.     

Tsga10 expression correlates with sperm profiles in the adult formalin‐exposed mice

Testis‐specific gene antigen10 (Tsga10), as a cytoskeletal protein in the sperm tail, impacts the sperm motility. This study investigates the correlation between sperm profile alterations and Tsga10 gene expression in adult mice exposed to formaldehyde (FA) and then treated with antioxidant effect of manganese (Mn²⁺). In this regard, we examined 35 NMRI adult male mice (6–8 weeks age) in 4 groups of control, sham, FA‐exposed and FA+Mn²⁺. The mice in FA+Mn²⁺ group were exposed to FA (10 mg kg^?1 twice a day) for 2 weeks and treated with daily Mn²⁺ administration (5 mg kg^?1) in the second week prior to sacrificing the mice for testis dissection. The right testis was dissected in each group and subjected to RNA extraction and cDNA syntheses for gene expression analysis by real‐time PCR. The findings revealed that FA decreased sperm parameters and Tsga10 expression (52.6 ± 24.37%). However, the injected powerful manganese antioxidant improved sperm profile through overexpression of Tsga10 (121.6 ± 27.13%) under FA‐induced stressful condition which proves the correlation between sperm profile and Tsga10 expression (P ≤ 0.05). This study also shows that Tsga10 expression protects sperm dysfunction in FA+Mn²⁺ group and resulting in better preservation of spermatozoa and improvement of male fertility.     

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.     

Tocotrienol‐rich fraction supplementation prevents foetal loss in females mated with corticosterone‐treated male Sprague–Dawley rats

This study examined whether tocotrienol supplementation to corticosterone‐treated male rats could prevent foetal loss in females upon their mating. Epididymides of adult male Sprague–Dawley (SD) rats with proven fertility were surgically separated at the testis‐caput junction. Twenty‐four hours post‐surgery, these animals received for 7 days either: tocopherol‐stripped corn oil (Control), corticosterone 25 mg/kg s.c. (CORT), CORT 25 mg/kg s.c. and tocotrienol‐rich fraction (TRF) 100 mg/kg orally (CORT + TRF) or TRF 100 mg/kg orally (TRF). On day 8, males were cohabited with proestrus females. A spermatozoa‐positive vaginal smear indicated pregnancy. Males were euthanised for analysis of testosterone and antioxidant activities. Reproductive organs were weighed. On day 8 of pregnancy, females were laparotomised to count the number of implantation sites. Pregnancy was continued until term. Number of pups delivered and their weights were determined. Data were analysed using ANOVA. Malondialdehyde levels were significantly lower in CORT + TRF group compared with CORT group. Enzymatic antioxidant activities, testosterone level and reproductive organ weights were significantly higher in CORT + TRF group compared with CORT group. Number of implantation sites and live pups delivered, and their birth weights from females mated with CORT + TRF males were significantly higher compared to CORT group. Therefore, TRF prevents foetal loss in females mated with CORT + TRF‐treated males.     

Vitamin E attenuates nicotine‐ and noise‐induced reproductive impairment in male albino Wistar rats

Previous studies showed that exposure to stress or nicotine induced reproductive impairment in male rats. Here, we assessed the effect of an antioxidant (vitamin E) on nicotine‐, stress‐ and nicotine + stress‐induced reproductive impairment in male rats. Forty‐eight male albino Wistar rats were divided into eight groups as follows; control, stress (generator noise 90–120 dB, 8 hr/day), nicotine (1.5 mg kg^?1 day^?1), nicotine + stress, vitamin E (100 mg kg^?1 day^?1), stress + vitamin E, nicotine + vitamin E and stress + nicotine + vitamin E. Sperm count, viability, motility and rapid progressive forward movement decreased significantly (p < 0.05), while percentage of nonmotile spermatozoa increased significantly (p < 0.05) in stress, nicotine and nicotine + stress groups, compared with control. Serum testosterone and follicle‐stimulating hormone decreased significantly (p < 0.05) in stress, nicotine and nicotine + stress groups, compared with control. Serum luteinising hormone decreased (p < 0.05) significantly in stress and nicotine + stress groups, compared with the control. Histology of the testes showed loss of germ cells in numerous seminiferous tubules, and epididymal histology showed decreased sperm density in stress, nicotine and nicotine + stress groups compared with the control. These negative changes were more severe in the nicotine + stress group. Vitamin E ameliorated the negative changes in the above parameters. This may be attributable to its antioxidant property.     

The effect of gadolinium‐based contrast agents on rat testis

Previous studies have reported that repeated administrations of linear gadolinium‐based contrast agents lead to their accumulation in the brain and other tissues in individuals with normal renal functions. The purpose of this prospective animal study was to investigate the effect of multiple administrations of macrocyclic ionic (gadoteric acid) and linear nonionic (gadodiamide) gadolinium‐based contrast agents (GBCAs) on rat testis tissue and to compare these molecules in terms of tissue damage. Thirty‐two male Sprague‐Dawley rats were kept without drugs for 5 weeks after administration of 0.1 mmol mg^?1 kg^?1 (0.2 ml/kg) gadodiamide and gadoteric acid for 4 days over 5 weeks. Biochemical, histopathological and immunohistochemical changes in testis tissue were evaluated at the end of 10 weeks. When used in repeated clinical doses, gadolinium was observed to increase apoptosis in the Leydig cells of the rat testis, and to increase serum Ca⁺² levels and reduce testosterone levels (p < .05). Although the difference was not statistically significant, a greater loss of spermatozoa and immature germinal cell accumulation were observed in the seminiferous tubule lumen in the GBCA groups compared with the control and saline groups (p > .05). Both linear and macrocyclic contrast agents have toxic effects on testis tissue, irrespective of the type of drug.     

Protective effect of alpha glucosyl hesperidin (G‐hesperidin) on chronic vanadium induced testicular toxicity and sperm nuclear DNA damage in male Sprague Dawley rats

The study was conducted to evaluate the vanadium‐induced testicular toxicity and its effect on sperm parameters, sperm nuclear DNA damage and histological alterations in Sprague Dawley rats and to assess the protective effect of G‐hesperidin against this damage. Treatment of rats with vanadium at a dose of 1 mg kg bw^?1 for 90 days resulted in significant reduction in serum testosterone levels, sperm count and motility. Further, a parallel increase in abnormal sperm morphology and adverse histopathological changes in testis was also associated with vanadium administration when compared to normal control. Moreover, sperm chromatin dispersion assay revealed that vanadium induces sperm nuclear DNA fragmentation. A marked increase in testicular malondialdehyde levels and decreased activity of antioxidant enzymes such as superoxide dismutase and catalase indicates vanadium‐induced oxidative stress. Co‐administration of G‐hesperidin at a dose of 25 and 50 mg kg bw^?1 significantly attenuated the sperm parameters and histological changes by restoring the antioxidant levels in rat testis. These results suggested that vanadium exposure caused reduced bioavailability of androgens to the tissue and increased free radical formation, thereby causing structural and functional changes in spermatozoa. G‐hesperidin exhibited antioxidant effect by protecting the rat testis against vanadium‐induced oxidative damage, further ensures antioxidant potential of bioflavonoids.