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Alcohol Withdrawal and Brain Injuries: Beyond Classical Mechanisms

Department of Pharmacology and Neuroscience, University of North Texas Health Science Center at Fort Worth, 3500 Camp Bowie Blvd., Fort Worth, TX 76107-2699, USA
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Molecules 2010, 15(7), 4984-5011; https://doi.org/10.3390/molecules15074984
Received: 30 April 2010 / Revised: 15 July 2010 / Accepted: 19 July 2010 / Published: 20 July 2010
(This article belongs to the Special Issue Neuroprotective Strategies)
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, 17β-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. View Full-Text
Keywords: antioxidant; brain aging; 17β-estradiol; ethanol withdrawal; mitochondria; oxidative stress; protein kinase; protein oxidation antioxidant; brain aging; 17β-estradiol; ethanol withdrawal; mitochondria; oxidative stress; protein kinase; protein oxidation
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Jung, M.E.; Metzger, D.B. Alcohol Withdrawal and Brain Injuries: Beyond Classical Mechanisms. Molecules 2010, 15, 4984-5011.

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