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Journal Article

Citation

Jung ME, Wilson AM, Metzger D, Brown ND, Simpkins JW. Alcohol Clin. Exp. Res. 2008; 32(6s1): 369A-369A.

Copyright

(Copyright © 2008, John Wiley and Sons)

DOI

10.1111/j.1530-0277.2008.00689_12.x

PMID

unavailable

Abstract

We have demonstrated that abrupt termination of chronic ethanol diet creates lipid peroxidation in young adult rats in a manner protected by endogenous estrogen [(17(-estradiol (E2)]. In this study, we tested whether ovariectomy exacerbates a deleterious interaction between ethanol withdrawal (EW) and age at the levels of oxidative stress using a 3 month ethanol diet paradigm. 5-, 12-, and 16-month-old ovariectomized rats with oil pellet or E2 replacement received a liquid ethanol (6.5%) or control dextrin diet for 3 months. One group was terminated from the ethanol diet by step-down concentrations of ethanol. Another group was terminated from the ethanol diet abruptly. Cerebellum, cortex, hippocampus were collected to assess the levels of carbonyls as a marker of oxidative damage to protein. Compared to groups with control dextrin diet and gradual termination of ethanol diet, EW groups showed a greater increase in protein carbonyls. Such phenomenon was more profound in older rats vs younger rats and more profound in ovariectomized rats vs in ovary intact rats. This increase in carbonyl contents was partially prevented by E2 implantation. These findings suggest that ovariectomy sensitizes brain to a deleterious interaction of EW with age in a manner that is more prominent after abrupt termination than a gradual termination of ethanol of long term ethanol diet (supported by NIAAA AA013864 and AA015982).

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