Download The Consequences of Alcoholism: Medical Neuropsychiatric by Marc Galanter PDF

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By Marc Galanter

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102 In vitro, metabolism of acetaldehyde via xanthine oxidase or aldehyde oxidase may generate free radicals, but the concentration of acetaldehyde required is much too high for this mechanism to be of significance in vivo. However, another mechanism to promote lipid peroxidation is via GSH depletion. One of the three amino acids of this tripeptide is cysteine. Binding of acetaldehyde with cysteine and/or glutathione (GSH) (Fig. 104 GSH is selectively depleted in the mitochondria65 and may contribute to the striking alcohol-induced alterations of that organelle.

3. 134 20 I • Medical Consequences 4. 1 kcal/g). It is almost as energy-dense as fat and more energy-dense than carbohydrates or proteins. In many societies, alcoholic beverages are considered part of the food supply, whereas in others, alcohol is consumed mainly for its mood-altering effects. In the alcoholic, alcohol represents on the average 50% of the total dietary energy intake; as a consequence, alcohol displaces many normal nutrients in the diets, resulting in primary malnutrition and associated symptomatology, foremost that of folate, thiamine, and other vitamin B deficiencies.

1c. Vitamin E and Miscellaneous Other Antioxidants. 179 reported a reduced hepatic α-tocopherol content after chronic ethanol feeding 24 I • Medical Consequences in rats receiving adequate amounts of vitamin E, as well as in the blood of alcoholics. Hepatic lipid peroxidation was significantly increased after chronic ethanol feeding in rats receiving a low vitamin E diet,180 indicating that dietary vitamin E is an important determinant of hepatic lipid peroxidation induced by chronic ethanol feeding.

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