Increased vulnerability of brain to estrogen withdrawal-induced mitochondrial dysfunction with aging

J Bioenerg Biomembr. 2008 Dec;40(6):625-30. doi: 10.1007/s10863-008-9195-1. Epub 2009 Jan 13.

Abstract

In the present study, to determine whether aging could increase the vulnerability of the brain to estrogen withdrawal-induced mitochondrial dysfunction, we measured the cytochrome c oxidase (COX) activity and mitochondrial adenosine triphosphate (ATP) content in hippocampi of 2 groups of ovariectomized (OVX) Wistar rats aged 2 months (young) and 9 months (middle-aged), respectively. In addition, effects of genistein and estradiol benzoate (EB) were tested also. We observed only a transient alteration of COX activity and mitochondrial ATP content in hippocampi of young OVX rats but a prolonged lowering of COX activity and mitochondrial ATP content in hippocampi of middle-aged OVX rats. This suggested that with aging compensatory mechanisms of mitochondrial function were attenuated, thus exacerbated estrogen withdrawal-induced mitochondrial dysfunction in hippocampi. Significantly, EB/genistein treatment reversed this estrogen withdrawal-induced mitochondrial dysfunction in both young and middle-aged rats suggesting that genistein may be used as a substitute for estradiol to prevent age-related disease such as Alzheimer's disease in post-menopausal females.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenosine Triphosphate / metabolism*
  • Aging / metabolism*
  • Animals
  • Estrogens / metabolism*
  • Female
  • Hippocampus / metabolism*
  • Mitochondria / metabolism*
  • Mitochondria / pathology*
  • Ovariectomy
  • Prostaglandin-Endoperoxide Synthases / metabolism*
  • Rats
  • Rats, Wistar

Substances

  • Estrogens
  • Adenosine Triphosphate
  • Prostaglandin-Endoperoxide Synthases