• Journal of Nutrition and Health
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• v.32 no.4
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• pp.376-383
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• 1999

The effects of $\beta$-carotene substitutionl for vitamin A and the chronic consumption of ethanol of ethanol on hepatic folate metabolism were studied it rats. The substitution of $\beta$-carotene for vitamin A depressed hepatic 10-formyl-tetreahydrofolate dehydrogenase(10-formyl-tetrahydrofolate : NADP oxidoreductase, E.C. 1.5. 1.6)activity to 65% of controls(p<0.001) and enhanced hepatic 5, 10-methy-lenetetrahydrofolate reductase(E. C. 6.3.3.2)activity by 56% with respect to control levels(p<0.001). Hepatic activity of 10-formyltertrahydrofolate dehydrogenase was depressed to about half that of control levels by ethanol administration to rats(36% ethanol diet, p<0.001). The activity of 5, 10-methyleneterahydrofolate reductase was not changed by ethanol consumption. The increased activity of 5, 10-methyleneterahydrofolate reductase and the decreased activity of 10-formyltetrahydrofolate dehydrogenase appeared to decrease the level of nonmethyl folate conezyme and the rate of one-carbon metabolism. Plasma homocysteine concentrations were significantly higher in rats fed ethanol(p<0.01) o $\beta$-carotene(p<0.001) than in controls, which suggests that increased activity of 5, 10-methylenetetrahydrofolate reductase can depress homocysteine metabolism. We concluded that dietary substitution of $\beta$-carotene for vitamin A or chronic administration of ethanol resulted in changes in the activity of hepatic folate-dependent enzymes, which could affect the distribution of folate derivatives, plasma homocysteine levels and one-carbon metabolism.

• Environmental Mutagens and Carcinogens
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• v.16 no.1
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• pp.13-18
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• 1996

One mechanism of free-radical production by ethanol is suggested to be through the intracellular conversion of XDH to XO by increased ratio of NADH to NAD. The major mechanism for physiological compensation of cytosolic NADH/NAD balance is the malate/aspartate shutfie. Therefore, it is important to develop the method to improve the efficiency of malate/aspartate shuttle in ethanol metabolism. In the present study, various amino acids and organic acid involved in the shuttle were tested for their functional efficiency in modulating shuttle in the ethanol-perfused rat liver. The rate of ethanol oxidation in the liver perfused with aspartate alone or aspartate in combination with pyruvate, respectively, was increased by about 10% compared to control liver, but not in the tissues perfused with glummate, cysteine or pyruvate alone. Though glummate, cysteine and pyravate did not affect the ethanol oxidation significanfiy, they showed some suppresive effect on the ethanol-induced radical generation monitored by protein carbonylation analysis. Among the tested components, aspartate is confirmed to be the most efficient as a metabolic regulator for both ethanol oxidation and ethanol-induced oxidative stress in our perfusion system. These effects of aspartate would result from NAD recycling by its supplementation through the coupled aspartate aminotransferase/malate dehydrogenase reactions and the malate-aspartate shuttle.

• Journal of Nutrition and Health
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• v.23 no.6
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• pp.443-450
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• 1990

Pregnant rats were fed liquid diet to determine the influence of maternal ethanol intake on maternal and pup liver copper when dietary copper was low. The diets, which contained either 0.75(low) or 3.75(control)mg copper/1 with or without 30% of kcal from ethanol, were fed throughout gestation and the first 15 days of lactation. maternal calorie intake and body weight were unaffected by dietary treatment. Ethanol intake depressed maternal liver copper concentration only when diet copper was low(interactive effect P<0.05). Although ethanol intake depressed total pup liver copper concentration regardless of dietary copper level, the interactive effect observed in maternal liver was reflected incopper content of the pup liver metallothionein fraction eluted from a Sephadex G-75 column. The zinc content of metallothionein was inversely related to copper content of metallothionein. Results suggest that pregnancy and lactation is a special period to develop a copper deficiency when low copper intake and ethanol ingestion are combined not only in mothers but also in their offspring.