Bednarek-Tupikowska G

Serum lipid peroxides and total antioxidant status in postmenopausal women on hormone replacement therapy

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.

Plasma cytokines in obese women with polycystic ovary syndrome, before and after metformin treatment.

Objectives. Most research confirms that metformin therapy has a positive influence on cardiovascular risk factors (CVRF) such as dyslipidemia, insulin resistance and hyperandrogenism in polycystic ovary syndrome (PCOS). The aims of the present study were to establish other CVRF, such as plasma adiponectin, tumor necrosis factor-α (TNFα), interleukin-6 (IL-6) and C-reactive protein (CRP) levels, in obese premenopausal women with PCOS and to investigate the effect of metformin treatment on these factors. Materials and methods. The study group consisted of 29 PCOS woman with body mass index (BMI) >25 kg/m2. They were treated over 6 months with 500 mg metformin twice daily. Twenty-nine healthy individuals matched for age and BMI were controls. Adiponectin, TNFα, IL-6 and CRP levels were examined in all PCOS (before and after treatment) and control women. Results. In the PCOS group significantly lower plasma adiponectin and TNFα 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.

Pro12Ala PPAR γ2 gene polymorphism in PCOS women: the role of compounds regulating satiety

Five to ten percent of women of reproductive age suffer from polycystic ovary syndrome (PCOS). Leptin, NPY, galanin, cholecystokinin (CCK) are involved in the regulation of eating behavior. PPARγ are receptors that are probably involved in hyperandrogenism. This study was designed to assess associations between the Pro12Ala PPARγ2 gene polymorphism and satiety factors in PCOS. Fifty-four PCOS women and 51 healthy women were studied. Leptin, NPY, galanin, CCK levels, and genetic studies to detect Pro12Ala PPARγ2 gene polymorphism were assessed. The leptin levels in the PCOS women carrying Pro12Ala genotype were higher than in those with Pro12Pro and Ala12Ala. The PCOS women had higher leptin and NPY levels and lower galanin levels. Obese PCOS patients had lower CCK levels. Conclusions: In the PCOS women, a single Ala allele may have a protective role as far as hyperleptinemia is concerned. The PCOS women may reveal a disrupted central leptin/NPY feedback loop with some shifts in food intake.

The influence of dehydroepiandrosterone on histology of selected organs in rabbits on an atherogenic diet.

The influence of dehydroepiandrosterone (DHEA) in fodder on the histology of selected organs in rabbits with induced hypercholesterolemia and in healthy rabbits was studied. Rabbits were randomly assigned into four groups: (1) control; (2) atherogenic diet; (3) atherogenic diet with addition of DHEA; (4) normal diet with addition of DHEA. After 12 weeks, the rabbits were bled. Tissue samples were collected, fixed in a 0.4% solution of buffered formalin, dehydrated and embedded in paraffin. Fragments of 5-7 microns were stained with hematoxylin and eosin as well as according to the van Gieson method. Histological analysis showed features of steatosis and intense degenerative changes in analyzed organs of animals from group 2, i.e. liver, kidneys, adrenal glands, lungs and bone. The degenerative changes in the group which in addition to a fat-rich diet received DHEA, were similar to group 2, but much less intense. Histological pictures of organs of the rabbits which received DHEA and normal diet did not differ significantly from the control group. In animals with experimental hyperlipidemia, DHEA acts protectively, decreasing degenerative changes in internal organs caused by an atherogenic diet. DHEA does not change the histological picture of organs in healthy animals.