Objective:The current study investigated the effects of clomiphene citrate on the hypothalamic-pituitary-testicular axis, steroidogenesis, sperm parameters, and testicular antioxidant enzyme activity of male Wistar rats submitted to lead acetate (Pb)-induced reproductive toxicity. Methods:Twenty adult male Wistar rats were divided into four groups of equal size as follows: Control; Clomid (0.35 mg/kg); Pb (10 mg/kg); and Clomid + Pb. Serum levels of follicle stimulating hormone (FSH), luteinizing hormone (LH), testosterone, testicular 17-β hydroxysteroid dehydrogenase (17-β HSD) activity, androgen receptors, catalase activity, superoxide dismutase (SOD), malondialdehyde (MDA), sperm motility, viability, counts and morphology were estimated after oral administration of Clomid and/or lead acetate for 35 consecutive days. Data were analyzed using ANOVA at p<0.05.Results:Lead acetate significantly decreased (p<0.05) serum LH and testosterone levels, testicular 17β-HSD activity, androgen receptor expression, sperm motility, viability, counts, catalase activity, and SOD when compared with controls. Abnormal sperm morphology and MDA were significantly increased (p<0.05) in the Pb group compared with controls. Clomid co-administrated with lead acetate significantly increased (p<0.05) serum LH, testosterone levels, testicular 17β-HSD, androgen receptor expression, sperm motility and viability when compared with the group given lead acetate.Conclusions:The present study suggests that clomiphene citrate may stimulate testicular testosterone synthesis, sperm motility and viability via luteinizing hormone in a context of lead acetate-induced reproductive toxicity.

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Background Heavy metals are well documented to induce reproductive toxicity. This study was designed to investigate the role of vitamin E and quercetin on reproductive toxicity mediated by lead acetate in male Wistar rats. Thirty male adult Wistar rats were grouped into six (n = 5 per group) as follows: Group 1 (Control); Group 2 and 3 were administered with 100 mg/kg vitamin E and quercetin, respectively; Group 4 was administered with 30 mg/kg lead acetate; Groups 5 and 6 received lead acetate with vitamin E and lead acetate with quercetin, respectively. Results Lead acetate significantly increased (p < 0.05) testicular malondialdehyde, nitric oxide, lead ion and abnormal sperm morphology, while testicular catalase, superoxide dismutase activities, calcium ion, zinc ion, serum follicle stimulating hormone, luteinizing hormone, testosterone, sperm count, motility, average path, curvilinear velocity, and sperm viability were significantly reduced (p < 0.05). The co-administration of lead acetate with vitamin E and quercetin significantly reversed (p < 0.05) the testicular level of malondialdehyde, nitric oxide, lead ion, abnormal sperm morphology, catalase superoxide dismutase activities, calcium ion, zinc ion, follicle stimulating hormone, luteinizing hormone, testosterone, sperm count, motility, average path velocity and sperm viability. Conclusions Vitamin E and quercetin attenuated the reproductive toxicity induced by lead acetate in the male Wistar rats, and this suggests that vitamin E and quercetin may serve as possible therapeutic agents in improving male reproductive functions in heavy metal toxicity.

Objective: Oxidative stress is a mechanism of cadmium-induced reproductive dysfunction. Carpolobia lutea is a free radical scavenger. Our study investigated the potential protective effects of Carpolobia lutea root methanol extract against cadmium-induced reproductive toxicity. Methods: We obtained the Carpolobia lutea root in Akure, and it was authenticated at the Forestry Research Institute of Nigeria (FRIN) herbarium, Ibadan, Nigeria, with FHI number 109784. We used Soxhlet extraction to obtain its methanol extract. We used thirty male Wistar rats (150-170g) in this study, (n=5 per group), and treated them as follows: Control (1 ml/kg normal saline), Cd (2 mg/kg), Cd+MCL (2 mg/kg+100 mg/kg), Cd+MCL (2 mg/kg+200 mg/kg), MCL (100 mg/kg), MCL (200 mg/kg). We administered Carpolobia lutea orally for 8 weeks. We administered a single dose of 2 mg/kg of cadmium intraperitoneally. We assessed the sperm profile using a computer-aided sperm analyzer. Under microscopy, we determined the sperm acrosome reaction and the DNA damage. We measured the seminal fructose level using spectrophotometry, and the data were analyzed using ANOVA at p <0.05. Results: Cd+MCL (2mg/kg+200 mg/kg) significantly increased sperm count (339.0±25.0 vs. 29.0±4.5 million/mL), motility (80.0±0.2 vs. 55.0±4.9%), viability (68.7±2.7 vs. 31.3±2.9%) and decreased abnormal sperm (28.3±1.7 vs. 43.3±2.5%), relative to the cadmium group. Cd+MCL (2mg/kg+200 mg/kg) significantly increased acrosome reaction (68.0±7.5 vs. 15.2±2.4%) and seminal fructose level (0.49±0.06 vs. 0.28±0.06 mmol/L) relative to the cadmium group. Cd+MCL (2mg/kg+200 mg/kg) significantly decreased sperm DNA damage (14.1±1.6 vs. 35.9±5.3%) in relation to the cadmium group. Conclusions: Carpolobia lutea root extract improves the sperm variables of rats exposed to cadmium.

The current study assessed the protective role of vitamin E in alleviating the detrimental effect of nicotine on reproductive functions in male rats. Twenty four male albino rats were divided into four groups of six rats. Control group was treated orally with 1.1 ml/kg body weight normal saline, nicotine treated group received 1.0 mg/kg body weight of nicotine, vitamin E treated group received 100 mg/kg body weight of vitamin E while nicotine plus vitamin E treated group received 1.0 mg/kg body weight of nicotine plus 100 mg/kg body weight of vitamin E. The administration of nicotine and vitamin E were done orally for 40 days. Nicotine caused a significant reduction (p<0.05) in sperm count, sperm motility, sperm viability and normal sperm cells. It also caused a significant reduction (p<0.05) in serum testosterone, follicle stimulating hormone and luteinizing hormone levels. There was impairment in testicular histology of rats treated with nicotine. Vitamin E improved the reduction in sperm characteristics, hormone levels and testicular alterations observed in nicotine treated rats. The study shows that nicotine exerts significant deleterious effects on male reproductive system and the concurrent administration of vitamin E ameliorated these detrimental effects.