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.
Molecules. 2010 Jul 20;15(7):4984-5011. doi: 10.3390/molecules15074984.
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 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.
未得到妥善处理的、由过度饮酒（乙醇）导致的突然戒断，会对小脑、海马体或大脑皮层等脆弱脑区的神经元完整性造成负面影响。除了众所周知的兴奋性神经传递之外，乙醇戒断（EW）还会引发活性氧（ROS）的大量产生和应激反应蛋白激酶的激活，这些都是本文的重点关注内容。EW 还会损害线粒体膜/膜电位，扰乱氧化还原平衡，并抑制线粒体酶，所有这些都会损害线粒体的基本功能。此外，EW 会引发与年龄相关的应激。易受 EW 应激影响的脆弱年龄段不一定是最年长的年龄段，并且因 EW 的目标分子而异。一种主要的女性性激素，17β-雌二醇（E2），会干扰 EW 诱导的氧化信号通路改变，从而保护神经元、线粒体和行为。本综述试图提供 EW 引发脑损伤和 E2 对此进行保护的氧化信号机制的综合信息。
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