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

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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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Authors and Affiliations

  1. Department of Anatomy, Zhongshan Medical College, Sun Yat-Sen University, Guangzhou, Guangdong, 510080, China

    Chun Shi & Jie Xu

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  1. Chun Shi
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  2. Jie Xu
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Correspondence to Jie Xu.

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Shi, C., Xu, J. Increased vulnerability of brain to estrogen withdrawal-induced mitochondrial dysfunction with aging. J Bioenerg Biomembr 40, 625–630 (2008). https://doi.org/10.1007/s10863-008-9195-1

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  • DOI: https://doi.org/10.1007/s10863-008-9195-1

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