The inhibition of low density lipoprotein oxidation by 17-alpha estradiol

Exp Clin Endocrinol Diabetes. 1999;107(1):53-7. doi: 10.1055/s-0029-1212073.

Abstract

The inhibition of LDL-oxidation by 17-alpha estradiol was assessed in vitro by the determination of the duration of the lag-phase in copper ion-induced oxidation and compared to that of 17-beta estradiol, estriol, and probucol. Addition of 0.2, 0.4, and 1 micromol/l of the test substances prolonged the lag-phase of LDL-oxidation 1.3-(+/-0.09 SD), 1.7-(+/-0.14 SD), and 2.7-(+/-0.25 SD) fold for 17-alpha estradiol; 1.4-(+/-0.14 SD), 1.8-(+/-0.1 SD), and 2.6-(+/-0.16 SD) fold for 17-beta estradiol; 1.1-(+/-0.07 SD), 1.4-(+/-0.11 SD), and 1.6-(+/-0.11 SD) fold for estriol as well as 1.4-(+/-0.14 SD), 1.6-(+/-0.1 SD), and 3.0-(+/-0.21) fold for probucol, thus proving that 17-alpha estradiol is as effective as 17-beta estradiol or similar to probucol and more effective than estriol (n = 6 in all cases). These data demonstrate that 17-alpha estradiol is able to delay LDL-oxidation, hence providing a basis for clinical examination of the protective effects of 17-alpha estradiol against atherosclerosis in patients where hormonal effects of 17-beta estradiol are undesirable.

MeSH terms

  • Antioxidants / pharmacology*
  • Copper / pharmacology
  • Estradiol / pharmacology*
  • Estriol / pharmacology
  • Humans
  • Lipoproteins, LDL / metabolism*
  • Male
  • Oxidation-Reduction
  • Probucol / pharmacology
  • Time Factors

Substances

  • Antioxidants
  • Lipoproteins, LDL
  • Estradiol
  • Copper
  • Estriol
  • Probucol