Can Coenzyme Q10 supplementation protect the ovarian reserve against oxidative damage?

PURPOSE: We investigated antioxidant effects of CoQ10 supplementation on the prevention of OS-induced ovarian damage and to evaluate the protective effect of such supplementation against OS-related DNA damage. METHODS: Twenty-four adult female Sprague-Dawley rats were randomly divided into three groups (8 rats per group): group 1 (control): saline, ip, and orally; group 2 (cisplatin group): cisplatin, 4.5 mg/kg ip, two times with an interval of 7 days; and group 3 (cisplatin + CoQ10 group): cisplatin, 4.5 mg/kg ip, two times with an interval of 7 days, and 24 h before cisplatin, 150 mg/kg/day orally in 1 mL of saline daily for 14 days. Serum concentrations of anti-Mullerian hormone (AMH), number of AMH-positive follicles, the assessment of the intensity of 8'OHdG immunoreactivity, the primordial, antral and atretic follicle counts in the ovary were assessed. RESULT(S): The mean serum AMH concentrations were 1.3 ± 0.19, 0.16 ± 0.03, and 0.27 ± 0.20 ng/mL in groups 1, 2, and 3, respectively (p < 0.01). Serum AMH levels were significantly higher in group 1 compared to groups 2 and 3 (p < 0.01 and p = 0.01, respectively). There was a statistically significant difference in AMH-positive follicle count between the groups (p < 0.01). Group 1 showed higher numbers of AMH-positive granulosa cells compared to group 2 (p = 0.01). A significant difference was found in the primordial, the atretic, and antral follicle counts between the three groups (p < 0.01, p < 0.01, and p < 0.01, respectively). The atretic follicle count was significantly lower in the cisplatin plus CoQ10 group compared to the cisplatin group (p < 0.01). The antral follicle counts were significantly higher in the cisplatin plus CoQ10 group compared with the cisplatin group (p < 0.01). There was a statistically significant difference in the intensity of staining of the follicles that were positive for anti-8'OHdG between the groups (p = 0.02). Group 1 showed a significant lower intensity of staining of the follicles positive for anti-8'OHdG compared with group 2 (p = 0.03). CONCLUSION(S): CoQ10 supplementation may protect ovarian reserve by counteracting both mitochondrial ovarian ageing and physiological programmed ovarian ageing although the certain effect of OS in female infertility is not clearly known.

The effects of letrozole and melatonin on surgically induced endometriosis in a rat model: a preliminary study.

OBJECTIVE: To determine the effects of letrozole and melatonin on surgically induced endometriosis in a rat endometriosis model. DESIGN: Prospective, randomized, controlled, experimental study. SETTING: Experimental Research Center of Yeditepe University (YUDETAM). ANIMAL(S): Thirty female, nonpregnant, nulligravid Wistar-Hannover albino rats. INTERVENTION(S): Surgical induction of endometriosis, administration of estrogen for 2 weeks, and laparotomy; administration of letrozole or melatonin for 2 weeks after induction of endometriosis, and laparotomy; administration of estrogen for 2 weeks and necropsy. MAIN OUTCOME MEASURE(S): The volume and histopathologic scores of endometriotic foci, and levels of superoxide dismutase, catalase, and malondialdehyde in the peritoneal fluid. RESULT(S): The mean volumes of the endometriotic foci were 99.6 +/- 18.8 mm(3), 21.5 +/- 7.4 mm(3), and 29.2 +/- 17.5 mm(3), and histopathologic scores were 2.5 +/- 0.7, 2.0 +/- 0.8, and 1.7 +/- 0.9 in the melatonin group at the end of the second, fourth, and sixth weeks, respectively. The mean volumes of the endometriotic foci were 75.9 +/- 26.3 mm(3), 29.8 +/- 14.7 mm(3), and 121.2 +/- 35.1 mm(3) and the histopathologic scores were 2.5 +/- 0.5, 2.2 +/- 0.8, and 2.7 +/- 0.4 in the letrozole group at the end of the second, fourth, and sixth weeks, respectively. In the melatonin group, peritoneal fluid superoxide dismutase and catalase levels increased statistically significantly. CONCLUSION(S): Melatonin caused more pronounced regression of endometriotic foci when compared with letrozole in a rat model. After the cessation of melatonin treatment, the recurrence rate was lower than that observed after the cessation of letrozole treatment.