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Objectives To evaluate the effects of inhibiting nitric oxide synthase as a means of intervention in nicotine-induced infertility in male rats. Methods Forty-eight male and thirty female Wistar rats (180–200 g) were randomly assigned to six groups and treated orally for 30 days with saline (control), nicotine (0.5 mg/kg, 1.0 mg/kg) with or without NG Nitro- l -Arginine Methyl Ester ( l -NAME, 50 mg/kg). Treated male rats were cohabited with untreated females in ratio 1:2 for fertility studies. Sperm analysis was done by microscopy. Results There was a significant decrease in the epididymal sperm motility and count after nicotine treatment. However, the percentage of abnormality significantly increased in nicotine treatment groups. Fertility studies revealed that nicotine reduced libido in male rats and decreased litter weight and number delivered by the untreated female during the experiments. Co-treatment with l -NAME effectively reversed the nicotine-mediated alterations in the sperm functional parameters, fertility indexes and hormone when compared to nicotine only. Conclusion Taken together, the present data indicate the abilities of l -NAME to ameliorate nicotine-induced spermatotoxic effects in male rats via a mechanism dependent on the circulating testosterone level.

Background: The administration of nicotine is associated with altered hormonal imbalances and increased serum and testicular nitric oxide (NO) level. Aim: This study sought to investigate the effects of NO inhibition with NG -nitro-L-arginine methyl ester (L-NAME) on altered hormonal imbalance in adult male albinorats. Materials and Methods: Rats were administered with 0.5 mg/kg body weight (BW) and 1.0 mg/kg BW nicotine and were treated with L-NAME in the drinking water or drinking water alone for 30 days. Serum was analyzed for testosterone, luteinizing hormone (LH), follicle stimulating hormone (FSH), and prolactin using radioimmunoassay. Results: Nicotine administration significantly decreased (P < 0.05) testosterone in the low and high dose treated groups and FSH in the high dose treated group when compared with the control group. There was a significant increase (P < 0.05) in mean LH and prolactin level in the high dose treated group when compared with the control. Concomitant treatment with nicotine and L-NAME produced significant increases in testosterone and FSH, and a decrease in prolactin in 1.0 mg/kg BW. L-NAME alone did not lead to a significant increase in testosterone when compared with control. Conclusion: These data demonstrate that the suppressive effects of nicotine on testosterone level of the adult male rat can be prevented by NOS blockade with L-NAME. It appears that these beneficial effects are mediated primarily within the gonad; however, the involvement of the pituitary cannot be totally ruled out.

Background: Oxidative stress has repeatedly been implicated as the leading cause of several disease conditions. Aim: This study was designed to investigate the effects of nicotine administration on serum antioxidant levels in male albino rats. Materials and Methods: Forty male rats (150-180 g) were divided into five groups and treated orally for 30 days. Group I (control) received 0.2 ml/kg normal saline and Groups II and III received 0.5 and 1.0 mg/kg body weight (BW) of nicotine, respectively for 30 days. The fourth and fifth groups were administered with 0.5 and 1.0 mg/kg BW of nicotine for 30 days, but were left untreated for another 30 days. Serum was assayed for nitric oxide (NO), lipid peroxidation, and antioxidant enzyme. Results: The levels of superoxide dismutase (SOD) and catalase (CAT) were significantly decreased (P < 0.05) in 0.5 and 1.0 mg/kg nicotine treated groups. Glutathione peroxidase (GPx) and glutathione reductase (GR) were significantly decreased (P < 0.05), while NO and malondialdehyde (MDA) were significantly increased (P < 0.05) in 1.0 mg/kg treated group when compared with the control. Conclusion: The present study shows that nicotine administration is associated with decreased serum antioxidant and increase lipid peroxidation ameliorated by nicotine withdrawal in male rat.

Objectives: Nicotine intake has been associated with reduced fertility, although the mechanisms responsible are still unclear. However, oxidative stress has been repeatedly implicated as the leading cause of male infertility. This study was therefore designed to investigate the effects of nicotine administration on testicular oxidant and antioxidant system in male albino rats. Materials and Methods: Forty male rats weighing between 150 and 180 g were divided into five groups and treated orally for 30 days. Group I, which served as the control received 0.2 ml/kg normal saline, Groups II and III received 0.5 mg/kg and 1.0 mg/kg body weight (BW) of nicotine respectively. The fourth and fifth groups were administered with 0.5 mg/kg and 1.0 mg/kg BW of nicotine, but were left untreated for another 30 days. Homogenate of testis and epididymis were assayed for lipid peroxidation and anti-oxidant enzyme. Results: The results show a significant decrease (P < 0.05) in testicular glutathione peroxidase, glutathione reductase, catalase and superoxide dismutase while a significant increase (P < 0.05) was observed in testicular lipid peroxidation and nitric oxide level in both groups when compared with the control. Conclusion: This experiment established that nicotine administration is associated with decreased testicular antioxidant and increase testicular lipid peroxidation, which might be a mechanism by which nicotine induce infertility.

OBJECTIVES: The use of nicotine through smoking remains a serious health problem. It has been associated with reduced fertility, although the mechanism responsible is still unclear. The present study was designed to investigate whether nicotine-induced infertility is associated with altered male reproductive hormones in male albino rats. MATERIALS AND METHODS: Forty male rats were divided equally into five groups and treated orally for thirty days. Group I, which served as the control received 0.2 ml/kg normal saline, Group II and III received 0.5 mg/kg (low dose) and 1.0 mg/kg (high dose) body weight of nicotine, respectively. The fourth and fifth groups were gavaged with 0.5 mg/kg and 1.0 mg/kg body weight of nicotine but were left untreated for another 30 days. These groups served as the recovery groups. Serum was analyzed for testosterone, luteinizing hormone (LH), follicle stimulating hormones (FSH), and prolactin using radioimmunoassay. RESULTS: Results showed that nicotine administration significantly decreased (P < 0.05) testosterone in the low and high treated groups and FSH in the high dose treated group when compared with the control group. There was a significant increase (P < 0.05) in mean LH and prolactin level in the high dose treated group when compared with the control. However, the values of the recovery groups were comparable with the control. CONCLUSION: The findings in this study suggest that nicotine administration is associated with distorted reproductive hormones in male rats although ameliorated by nicotine cessation. It is plausible that the decreased testosterone level is associated with testicular dysfunction rather than a pituitary disorder.