Alcohol withdrawal and brain injuries: beyond classical mechanisms.

Molecules : a Journal of Synthetic Chemistry and Natural Product Chemistry
Marianna E Jung, Daniel B Metzger

Abstract

Unmanaged sudden withdrawal from the excessive consumption of alcohol (ethanol) adversely alters neuronal integrity in vulnerable brain regions such as the cerebellum, hippocampus, or cortex. In addition to well known hyperexcitatory neurotransmissions, ethanol withdrawal (EW) provokes the intense generation of reactive oxygen species (ROS) and the activation of stress-responding protein kinases, which are the focus of this review article. EW also inflicts mitochondrial membranes/membrane potential, perturbs redox balance, and suppresses mitochondrial enzymes, all of which impair a fundamental function of mitochondria. Moreover, EW acts as an age-provoking stressor. The vulnerable age to EW stress is not necessarily the oldest age and varies depending upon the target molecule of EW. A major female sex steroid, 17beta-estradiol (E2), interferes with the EW-induced alteration of oxidative signaling pathways and thereby protects neurons, mitochondria, and behaviors. The current review attempts to provide integrated information at the levels of oxidative signaling mechanisms by which EW provokes brain injuries and E2 protects against it. Unmanaged sudden withdrawal from the excessive consumption of alcohol (ethanol) adversely alter...Continue Reading

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Citations

Mar 2, 2016·Alcoholism, Clinical and Experimental Research·Ricardo Abadie-GuedesRubem Carlos Araújo Guedes
Apr 6, 2011·Alcoholism, Clinical and Experimental Research·Roberta ZanardiniLuisella Bocchio-Chiavetto
Oct 18, 2018·Oxidative Medicine and Cellular Longevity·Luanna Melo Pereira FernandesCristiane Socorro Ferraz Maia

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