Zinc deficiency as a mediator of toxic effects of alcohol abuse.

摘要: To review data on the role of ethanol-induced alteration Zn homeostasis in mediation adverse effects alcohol abuse. The scholarly published articles association between metabolism and alcohol-associated disorders (liver, brain, lung, gut dysfunction, fetal syndrome) have been reviewed. It is demonstrated that alcohol-induced modulation zinc transporters results decreased levels lungs, liver, gut, brain. deficiency increased permeability, ultimately leading to endotoxemia systemic inflammation. Similarly, lung epithelia alveolar macrophages decreases barrier function resulting respiratory distress syndrome. In turn, significantly contributes proinflammatory state alcoholic liver disease. Finally, impaired functions may play a significant brain damage, being associated with both signaling accumulation neurotoxic metabolites. also hypothesized interfere neurotransmission. Similar changes take place fetus as result placental transfer, maternal deficiency, or sequestration, Therefore, not only mediates ethanol exposure, but provides an additional link different disorders. Generally, current findings suggest assessment status could be used diagnostic marker metabolic disturbances abuse, whereas potential tool treatment