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.

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Summary: It has been emphasized that cigarette smoking is not always synonymous with nicotine administration but the toxic effect of cigarette has often been associated with the nicotine content in cigarette. Epidemiologic studies have clearly indicated that cigarette smoking have many deleterious effects on visceral tissues in women. However it is not certain whether this effect is produced entirely by nicotine as cigarettes contain other toxic substances. Using an animal model the direct effect of nicotine administration on viscera tissues in female albino rats was investigated. Twenty-four female rats with regular oestrous cycle in the same phase of the cycle were divided into two equal groups with each group receiving 0.5mg/kg nicotine and 0.9% normal saline S.C. daily respectively. Six rats from each group were killed by cervical dissociation after 30 and 60 days treatment. The ovary, uterus, brain, kidney, heart, adrenal, pituitary and the liver were removed weighed and histological study carried out. Weights of the ovary, kidney, pituitary and uterus were significantly reduced (P< 0.05) following nicotine treatment while weights of the heart and liver increased with 60days treatment with the appearance of cartilaginous cells in the heart and deposition of adipose around the portal vein in the liver. Necrosis, congestion, fibrosis, follicular and endometrial degeneration were observed in the brain, pituitary, kidney, ovary and uterus respectively. No significant difference between the weekly growth rates in nicotine treated (5.13 ± .29) and control (5.25 ± 0.18) animals. Nicotine has deleterious effects on some vital visceral organs with observations similar to those reported in women smokers.

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 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.