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

Journal of Bioenergetics and Biomembranes
Chun Shi, Jie Xu

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.

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Citations

Oct 14, 2009·Biochemical Pharmacology·Anna AtlanteSalvatore Passarella
Jul 16, 2010·Neurological Research·Yan HouGeng-Tao Liu
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Mar 12, 2021·Brain and Behavior·Xiaoying DuanHong Ding

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