Alcohol and Trace Elements in the Brain

Abstract

When men drink excessive amounts of alcohol over a prolonged period, they may develop neurological diseases, such as peripheral neuropathy, Wernicke encephalopathy, and alcohol-induced cerebellar degeneration. Trace elements in the brain can lead to the increased expression of receptors, enzymes for the synthesis and metabolism of the neurotransmitter, and proteins that modulate function, ets. It is possible that various neurological symptoms occur when trace elements in the brain are affected by excessive consumption of alcohol, even though the trace elements in the brain are maintained at a constant level. Drinking excessive levels of alcohol increases the level of zinc in the brain, while lower levels of zinc in blood are seen in men with signs of chronic excessive alcohol consumption, such as with alcoholic cirrhosis. It is speculated that increased free radicals by acute alcoholic intake, cause zinc to be increased in the brain in response to this phenomenon. Copper is closely related to neurological diseases, such as Wilson′s disease or Menkes disease, but there have been no reports regarding encephalopathy induced by changes in copper and its metabolites in the brain due to drinking. About 80% of manganese in the brain exists within the astrocytes, and is involved in glutamine metabolism. However, there have not been many reports concerning the relation between alcohol and manganese. Low levels of manganese in the blood are observed in chronic alcoholics and these patients exhibit delirium tremens, tetany, convulsions, athetosis and involuntary movement. The level of iron in the blood increases with chronic excessive alcohol drinking, but there have been no reports indicating that iron levels in the brain are modified by alcohol intake. Metal-lothionein (MT) contributes significantly to zinc and copper metabolism and functions as a protective protein, but MT in the brain is increased when the MT-I overexpressing transgenic mouse (MT-I*) is administered 4 g/kg of ethanol by a gastric tube. Acute ethanol administration can generate oxygen free radicals and cause oxidative stress in the brain. The mechanism of induction of MT in the brain after oral ethanol administration may be associated with oxidative stress caused by ethanol or its metabolites, and can be considered a protective mechanism against ethanol toxicity.