TRANSDERMAL ESTRADIOL AND MEDROXYPROGESTERONE ACETATE IN HORMONE REPLACEMENT THERAPY ARE BOTH ANTIOXIDANTS

被引：47

作者：

TRANQUILLI, AL ^{[1
]}

MAZZANTI, L ^{[1
]}

CUGINI, AM ^{[1
]}

CESTER, N ^{[1
]}

GARZETTI, GG ^{[1
]}

ROMANINI, C ^{[1
]}

机构：

[1] UNIV ANCONA,DEPT OBSTET & GYNECOL,ANCONA,ITALY

来源：

GYNECOLOGICAL ENDOCRINOLOGY | 1995年 / 9卷 / 02期

关键词：

ESTRADIOL; MEDROXYPROGESTERONE ACETATE; HRT; LIPID MEMBRANE; OXYGEN FREE RADICALS; MENOPAUSE; ESTROGENS;

D O I：

10.3109/09513599509160203

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

We have evaluated the effects of the different components of hormone replacement therapy (HRT) on the production of free radicals in platelet membranes from menopausal women. The study included 12 women in menopause for at least 6 months to a maximum of 4 years. First, the effect was determined of progestin only during the administration of 20 mg/day medroxyprogesterone acetate for 5 days. The peroxide production level was measured on day 0 and day 5. The second set of experiments was carried out in the first month of cyclic HRT with transdermal estradiol 50 mu g/day from day 1 to day 25 and medroxyprogesterone acetate from day 13 to day 25. In this experiment, the peroxide level was evaluated on days 0, 12 and 25. A significant reduction of peroxide level was observed after oval medroxyprogesterone acetate administration. During HRT, we observed a similar reduction in lipid oxidation at the peak of the estrogen effect, and a further decrease with the administration of medroxyprogesterone acetate. It is concluded that reduction of lipid peroxidation during HRT is not only due to estrogens, but also depends upon the combined action of sex steroids. This observation justifies not only the combined regimen (estrogens plus progestin) in HRT, but also the positive effects of progestins alone on patients who cannot use estrogens.

引用

页码：137 / 141

页数：5

共 25 条

[1]

Kay M.M., Bosman G.J., Shapiro S.S., Bendich A., Bassel P.S., Oxidation as a possible mechanism of cellular aging: vitamin E deficiency causes premature aging IgG binding to erythrocytes, Proc. Natl. Acad. Sci. USA, 83, pp. 2463-2467, (1986)

[2]

Loesser K.E., Kukreja R.C., Kazziha S.Y., Jesse R.L., Hess M.L., Oxidative damage to the myocardium: a fundamental mechanism of myocardial injury, Cardioscience, 4, pp. 199-216, (1991)

[3]

Halliwell B., Gutteridge J.M.C., Cross C.E., Free radicals antioxidants and human disease: where are we now?, J. Lab. Clin. Med, 119, pp. 598-620, (1992)

[4]

Stampfer M.J., Willett W.C., Colditz G.A., Rosner B., Speizer F.E., Hennekens C.H., A prospective study of postmenopausal estrogen therapy and coronary heart disease, N. Engl. J. Med, 313, pp. 1044-1049, (1985)

[5]

Sugioka K., Shimosegawa Y., Nakano M., Estrogens as natural antioxidants of membrane phospholipid peroxidation, FEBS Lett, 210, pp. 37-39, (1987)

[6]

Rodriguez del Castillo A., Battaner E., Guerra M., Alonso T., Mas M., Regional changes of brain Na+, K+-transporting adenosine triphosphatase related to ovarian function, Brain Res, 416, pp. 113-118, (1987)

[7]

Romanini C., Mazzanti L., Tranquilli A.L., Valensise H., Cester N., Effect of estriol on the transport of blood cells, Transvaginal Hormone Therapy in Climacteric Women, pp. 37-44, (1989)

[8]

Liehr J.G., Roy D., Free radical generation by redox cycling of estrogens, Free Rad. Biol. Med, 8, pp. 415-423, (1990)

[9]

Enouf J., Bredoux N., Bourdeau N., Sarkadi B., Levy-Toledano S., Further characterization of the plasma membrane and intracellular membrane-associated platelet Ca++ transport systems, Biochem. J, 263, pp. 547-552, (1989)

[10]

Rao G.H.R., Measurements of ionized calcium in normal human blood platelets, Anal. Biochem, 169, pp. 400-404, (1988)

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