In the PCOS group significantly lower plasma adiponectin and TNFalpha levels were observed, whereas there were no differences in plasma IL-6 and CRP levels between PCOS and control groups. Plasma adiponectin increased significantly after metformin treatment, but levels of inflammatory factors did not change.

Free radical reactions are involved in processes connected with aging. Estradiol acts as antioxidant and free radical scavenger, but the mechanism of this action remains unknown. Estradiol has a hydroxyphenolic structure and may donate hydrogen atoms to lipid peroxyradicals to terminate chain reactions. There are a few reports concerning the influence of estradiol on natural antioxidant enzyme activity, such as superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT). The aim of this study was to estimate the relationship between the levels of estradiol and lipid peroxide (LPO), a marker of membrane lipid peroxidation, and the correlation between estradiol and erythrocyte SOD and GSH-Px activity. The study included 13 premenopausal and 13 postmenopausal healthy women. Serum levels of estradiol, follicle-stimulating hormone (FSH) and LPO, and erythrocyte SOD and GSH-Px activity were estimated in all subjects. Premenopausal women revealed significantly higher estradiol levels and lower LPO concentrations, as well as significantly higher GSH-Px activity than the postmenopausal group. SOD activity did not differ between the two groups. There was a negative correlation between serum estradiol and LPO levels as well as a positive correlation between estradiol and GSH-Px activity. These results support the hypothesis that estradiol exerts its antioxidant action not only through its chemical structure but probably also through its influence on natural cellular antioxidant enzyme activity.

Estradiol (E2) has antioxidant properties. The role of progestins in antioxidant defense is still unknown. We have evaluated the influence of E2 and E2 plus medroxyprogesterone acetate (MPA) on serum lipid peroxide (LPO) levels, a marker of free radical reactions, and serum total antioxidant status (TAS) in postmenopausal women. Subjects consisted of 26 women with surgical menopause, before and after 4 months of estrogen replacement therapy (ERT; E2), and 54 women with natural menopause on hormone replacement therapy (HRT; E2 plus MPA). Forty premenopausal women served as a control group. Serum E2 was estimated by radioimmunoassay, follicle-stimulating hormone by IRMA methods, LPO and TAS by colorimetric methods. Before therapy, LPO levels in the postmenopausal women were significantly higher (p < 0.001) than in the control group. After both ERT and HRT, LPO decreased significantly and did not differ between both groups and the control group. TAS was significantly lower in postmenopausal women (p < 0.001) than in the control group before therapy. After both ERT and HRT, TAS increased significantly and did not differ between both groups and the control group. We conclude that oxidative stress is increased after menopause. ERT and HRT inhibit the generation of free radicals and raise antioxidant potential to the levels found in premenopausal women. MPA did not influence the antioxidant action of E2.

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