Abstract
Summary and conclusions
Release of folate from necrotic liver cells and its utilization during regeneration is responsible for reduction in liver content of folic acid and folinic acid in carbon tetrachloride-mduced liver injury. Superimposition of hepatic necrosis on dietary-induced folate depletion interferes with DNA synthesis and prevents or delays regeneration. Thymidine facilitates hepatic DNA synthesis in the presence of folate depletion, whereas, uracil and vit. B12 have no effect.
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