Dietary and pharmacological control of estradiol metabolism in humans

Ann N Y Acad Sci. 1990;595:291-9. doi: 10.1111/j.1749-6632.1990.tb34303.x.

Abstract

Clinical research has demonstrated that increased or decreased estradiol 2-hydroxylation can easily be achieved with a number of experimental approaches. In contrast, estradiol 16 alpha-hydroxylation, which may have potentially deleterious effects in estrogen-dependent tissues, cannot be readily altered. Predictable hormonal consequences have thus far been found in response to the modification of 2-hydroxylation. This approach offers promise as a method for specifically altering the risk for diseases associated with either too little estrogen (osteoporosis) or too much estrogen (breast and uterine cancer).

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Cimetidine / pharmacology
  • Cytochrome P-450 Enzyme System / metabolism
  • Diet
  • Estradiol / metabolism*
  • Female
  • Humans
  • Hydroxylation
  • Indoles / pharmacology
  • Menopause
  • Mice
  • Microsomes, Liver / metabolism
  • Plants, Toxic
  • Smoking
  • Steroid 16-alpha-Hydroxylase
  • Tobacco

Substances

  • Indoles
  • Estradiol
  • Cimetidine
  • Cytochrome P-450 Enzyme System
  • indole-3-carbinol
  • Steroid 16-alpha-Hydroxylase