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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.

The effects of T. occidentalis seed oil on some female reproductive indices were investigated in Wistar rats. The study was divided into two phases: (estrous cycle and pregnancy). Animals were grouped into four: group A received distilled water (control), groups B, C and D received 400, 600 and 800 mg/kg bw of T. occidentalis seed oil respectively. The pattern of estrous cycle was determined for three weeks before and during the treatment. Thereafter, each group was sub- divided into two. The sub-group-1 rats were mated with male breeders, the litter size and birth weight of their offsprings was determined. Sub-group-2 rats were sacrificed and histology of organs and serum levels of LH, FSH and estrogen were assayed. There was no significant difference between the pre-treatment and post-treatment estrous cycle length. However, there was a significant decrease in the frequency of diestrus phase during treatment in all the experimental groups when compared with pre-treatment period but there was no significant difference in the diestrus phase when compared with the control group. Serum estrogen concentration was significantly reduced in the group that was treated with 800 mg/kg bw of T. occidentalis seed oil. Histology of the ovary and uterus in the experimental groups were similar to that of the control group. Birth weight of pups was significantly increased in the group treated with 600 mg/kg bw of T. occidentalis seed oil when compared with the control group. The results of this study suggest that T. occidentalis seed oil does not alter estrous cycle in Wistar rats.

The crude methanol extract of the stem wood of Quassia amara . L. (A-1) significantly caused a reduction in the weight of the testis, epididymis and seminal vesicle, but an increase in that of the anterior pituitary gland. Epididymal sperm counts, serum levels of testosterone, luteinizing hormone (LH) and follicle stimulating hormone (FSH) were significantly reduced when the rats were treated with the extract. Furthermore the basal and LH-stimulated testosterone secretion of Leydig cells isolated from rats pretreated with the extract was inhibited. These changes seemed to be restored eight weeks after the withdrawal from extract treatments. Two compounds — quassin and 2-methoxycanthin-6-one were isolated after fractionation of A-1. Quassin produced similar biological actions as the crude extract while the effects of 2-methoxycanthin-6-one did not seem to differ from those of the control. Quassin appears to be the antifertility principle of Quassia amara .

The crude methanol extract of the stem wood of Quassia amara L. inhibited both the basal and LH-stimulated testosterone secretion of rat Leydig cells in a dose-dependent fashion. Fractionation of the extract by chromatography gave quassin (1) and 2-methoxycanthin-6-one (2); compound 1 proved to be the bioactive agent.