ABSTRACT
Nicotine as a toxic agent in cigarette smoke impairs the reproductive system. Sambucus ebulus extract (SEE) is shown to have some beneficial effects such as antioxidant properties. The aim of this study was to evaluate the effects of SEE on the hormones of the pituitary-gonadal axis, lipid peroxidation index, antioxidant enzymes, spermatogenesis, and epididymal sperm parameters in male mice treated with nicotine. Adult male mice were divided into five groups; A: normal saline, B: 1 mg/kg nicotine, C: 1 mg/kg nicotine and 10 mg/kg SEE, D: 1 mg/kg nicotine and 50 mg/kg SEE, D: 1 mg/kg nicotine and 100 mg/kg SEE. Treatments lasted for 35 days. The spermicidal activity of SEE was tested in vitro. Sperm count, motility and morphology were assessed for fertility. Serum testosterone, prolactin and luteinizing hormone (LH) were measured, using ELISA. Serum malondialdehyde (MDA), catalase (CAT), and superoxide dismutase (SOD) activity were measured, using colorimetric assays. Spermatogenesis was evaluated by Johnsen’s score and morphometry in histological slides. SEE at different doses did not have any spermicidal activity. Sperm parameters were reduced in the nicotine-treated group, compared with controls (P<0.01). Nicotine reduced testosterone and LH levels (P<0.01) and increased prolactin (P<0.01).A hike in MDA and a reduction in SOD activity without change on CAT, were observed in the nicotine group. Nicotine caused hypospermatogenesis. SEE improved most of the above-mentioned parameters, especially in the doses of 50 and 100 mg/kg. Beneficial effects of SEE in the doses of 50 and 100 mg/kg on male reproduction impairment, induced by nicotine might be partly attributed to the reduction of oxidative stress and changes in the hormones of the pituitary-gonadal axis.
ABSTRACT
Nicotine as a toxic agent in cigarette smoke impairs the reproductive system. Sambucus ebulus extract (SEE) is shown to have some beneficial effects such as antioxidant properties. The aim of this study was to evaluate the effects of SEE on the hormones of the pituitary-gonadal axis, lipid peroxidation index, antioxidant enzymes, spermatogenesis, and epididymal sperm parameters in male mice treated with nicotine. Adult male mice were divided into five groups; A: normal saline, B: 1 mg/kg nicotine, C: 1 mg/kg nicotine and 10 mg/kg SEE, D: 1 mg/kg nicotine and 50 mg/kg SEE, D: 1 mg/kg nicotine and 100 mg/kg SEE. Treatments lasted for 35 days. The spermicidal activity of SEE was tested in vitro. Sperm count, motility and morphology were assessed for fertility. Serum testosterone, prolactin and luteinizing hormone (LH) were measured, using ELISA. Serum malondialdehyde (MDA), catalase (CAT), and superoxide dismutase (SOD) activity were measured, using colorimetric assays. Spermatogenesis was evaluated by Johnsen’s score and morphometry in histological slides. SEE at different doses did not have any spermicidal activity. Sperm parameters were reduced in the nicotine-treated group, compared with controls (P<0.01). Nicotine reduced testosterone and LH levels (P<0.01) and increased prolactin (P<0.01).A hike in MDA and a reduction in SOD activity without change on CAT, were observed in the nicotine group. Nicotine caused hypospermatogenesis. SEE improved most of the above-mentioned parameters, especially in the doses of 50 and 100 mg/kg. Beneficial effects of SEE in the doses of 50 and 100 mg/kg on male reproduction impairment, induced by nicotine might be partly attributed to the reduction of oxidative stress and changes in the hormones of the pituitary-gonadal axis.
ABSTRACT
Nicotine exposure causes impaired fertility and ovarian dysfunction. The aim of this study was to investigate the possible protective role of melatonin, which is known as an antioxidant agent on altered ovarian functions upon nicotine exposure. A total of 32 female adult NMRI mice were divided randomly into four groups [n=8]. The control group received vehicle, while group 2 received nicotine [40 microg/kg] for 15 days and group 3 melatonin [10 mg/kg] for 5 days. Group 4 received both nicotine [40 microg/kg] and melatonin [10 mg/kg] for the same periods. All animals were treated intraperitoneally. After autopsy on the 16th day, histopathological and morphometrical examinations were performed and serum estradiol concentrations were measured. The data were analyzed using ANOVA and Tukey post hoc test. A value of p<0.05 was considered significant. Nicotine significantly reduced the number of pre-antral and antral follicles, as well as estradiol concentration compared to the control group [p<0.05]. However, the decrease in the number of primordial follicles was not significant in the nicotine treated group. A significant increase in the atretic follicles were observed in group 2 compared to the control group [p<0.05]. Moreover, melatonin caused a marked normalization in the number of ovarian follicles and estradiol levels in group 4 compared to group 2. The results from this study suggest that melatonin may have a protective effect against nicotine-induced ovarian changes on the number of different stages of follicle growth