• 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.

• Tuberculosis and Respiratory Diseases
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• v.64 no.6
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• pp.460-465
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• 2008

Incidences of pulmonary thromboembolism markedly increase with age. Risk factors of pulmonary thromboembolism are surgery, trauma, acute medical illness, immobilization, pregnancy, usage of hormone, and advanced age. In the cases of thrombomembolism occurred in young age, the possibility of thrombophilc state is needed to be investigated. Among many diseases or state associated thrombophilic state, homocyteinemia should be considered a cause of thromboembolism before fifth decade. Homocyteinemia is caused by deficiency of N-5-methyltetrahydrofolate, cystathionie ${\beta}$-synthase and vitamin B12. The presence of the mutation of 5,10-methyleneterahydrofolate lead to homocyteinemia by deficiency of N-5-methyltetrahydrofolate. Homocysteine is acknowledged the risk factor of cardiovascular event, and storke. Homocysteinemia can be the cause of thromboemboism via damaging endotheial cell. We present two cases of pulmonary thromboembolism in young age which seem to be associated with homocysteinemia precipitated by mutation of 5,10-methyleneterahydrofolate.