Serum estradiol 17-sulphate and lipid peroxides in late pregnancy

Abstract

Estradiol 17-sulphate is readily converted to 2-OH or 4-OH estradiol 17-sulphate. The latter two strongly antagonize lipid peroxidation, which may play certain roles during pregnancy, such as pregnancy-induced hypertension. Serum estradiol 1 7-sulphate during mid and late pregnancy was measured using a direct radioimmunoassay without hydrolysis, and the level increased as pregnancy progressed. The levels in the sixth (20\p=n-\23 weeks) and tenth months (36\p=n-\39 weeks) of gestation were 1.42\m=+-\0.04nmol/l (mean\m=+-\sd)and 3.43\m=+-\1.09nmol/l, respectively. The maternal venous levels before and at delivery and in the umbilical veins and artery were 3.38\m=+-\0.83,3.48\m=+-\1.53, 4.11 \ m=+-\ 1.40 and 4.30\m=+-\1.81 nmol/l, respectively. The latter two values were slightly higher than the former two. Estradiol 1 7-sulphate in maternal venous blood began to decrease around delivery. Serum lipid peroxides were measured using the method of Yagi. Estradiol 17-sulphate and lipid peroxides showed a simple regression slope (r= \m=-\0.548,p<0.05) during late pregnancy. These results suggest that estradiol 1 7-sulphate may be converted to 2-OH or 4-OH estradiol 1 7-sulphate, which act as lipid peroxide scavengers during pregnancy.Estrogen sulphates have been shown to be quantitatively the most important estrogens in the peripheral blood ( 1, 2), and may have physiological and pathological roles in humans. Estrone sulphate (E]-S) and sulphatase activity showed the possibility of some roles stimulating human breast cancer and endometrial cancer (3).Estradiol 17-sulphate (E2-17-S) is a unique estrogen sulphate derived from testosterone sulphate and not from estradiol-17 ß (E2) in humans (4, 5). It shows three peaks in human urine during the menstrual cycle (6). It is readily converted to 2-OH E2-l 7-S and/or 4-OH E2-l 7-S (7, 8), both of which are stable (7) and strongly antagonize lipid peroxidation (9). However, E2-l 7-S has not yet been measured in the peripheral circulation of humans. In this study, serum E2-17-S during mid and late pregnancy, at delivery and after delivery was measured by a direct radioimmunoassay (RIA). The serum E2-l 7-S and lipid peroxides were then compared in late pregnancy. Patients and methods ReagentsPreparation of E2-17-S (10) and [6, 7-sH] E2-17-S (32.5 Ci/mmol) (11) was carried out as described previously. Unlabelled conjugated and free steroids were purchased from Sigma (St Louis, MO). Organic solvents and chemicals were of analytical grade. AntiserumThe antiserum used was obtained from a rabbit immu¬ nized with E2-17-S-fC-61-bovine serum albumin conju¬ gate (12). The antibody has a high specificity for E2-17-S, exhibiting no more than 0.2% of cross reactivites for other steroids (Table 1). Collection of samplesBetween 9.00 and 13.00 peripheral venous blood samples were collected from pregnant women. Several hours prior to delivery, maternal peripheral venous blood samples were obtained. Matched samples of umbilical arterial and venous blood and maternal peripheral venous blood were o...

Serum 2-Hydroxyestradiol 17-Sulphate in Pregnancy.

“…The serum level of E2-17-S at 20-23 weeks and 36-39 weeks of gestation was 1.42 ± 0.04 (mean ± SD) and 3.42 ± 1.09 nmol/l, respectively [1]. In comparison with these levels, the serum level of 2-OH E2-17-S obtained in the present assay in mid-to late pregnancy was rather high.…”

“…Previously [1], the serum level of E2-17-S showed a significant negative regression line for that of lipid peroxides. E2-17-S itself antagonizes lipid peroxidation, but not very strongly.…”

“…we measured the serum level of estradiol 17-sulphate (E2-17-S), a sulphated estrogen, during late pregnancy by a direct radioimmunoassay [1]. E2-17-S is quickly metabolized in the body to 2-hydroxyestradiol 17-sulphate (2-OH E2-17-S) and/or 4-hydroxyestradiol 17-sulphate (4-OH E2-17-S) [2,3].…”

“…Both 2-OH E2-17-S and 4-OH E2-17-S are more stable forms than the free catechol estrogens (2-OH E2, 4-OH E2) [4] and strongly antagonize lipid peroxidation [5]. The serum level of E2-17-S showed a significant negative regression line with that of lipid peroxides in pregnancy [1]. In the case of pregnancy-induced hypertension (PIH), the serum levels of lipid peroxide was reported as higher than in un-complicated pregnancy [6].…”

Effect of Estrogen Replacement Therapy on Hepatic Triglyceride Lipase, Lipoprotein Lipase and Lipids Including Apolipoprotein E in Climacteric and Elderly Women.

“…Estrogens, especially, estradiol 17-sulfate (E2-17-S) and its catecholized form, E2-17-S (2-OH E2-17-S, 4-OH E2-17-S), strongly suppress lipid peroxidation [23]. These estrogens may protect human arterial endothelial cells from oxidative stress, and may inhibit oxidation (oxidizing degeneration)…”