Abstract
Heme biosynthesis defect in vitamin E-deficient rats affecting bone marrow synthesis of delta- aminolevolinic acid and liver formation of porphobilinogen
Highlights
Vitamin E deficiency in the rat leads to decreased activities of bone marrow &aminolevulinic acid synthase and hepatic d-aminolevulinic acid dehydratase
The nature of the effect is highly specific as indicated by the observation that nonheme enzymes such as tissue ATPase, mitochondrial ATPase, malate, and isocitrate dehydrogenase, microsomal NADPH-cytochrome c reductase, and cytoplasmic glucose-6-P dehydrogenase remain unaltered in vitamin
The results presented here show that vitamin E deficiency leads to a decrease in the ability of the bone marrow to synthesize &aminolevulinic acid
Summary
Vitamin E deficiency in the rat leads to decreased activities of bone marrow &aminolevulinic acid synthase and hepatic d-aminolevulinic acid dehydratase. Studies on the incorporation of radioactivity from glycine-2J4C and &arninolevulinic acid-4J4C into bone marrow heme show that the defect in this tissue is at the level of the first enzyme, &aminolevulinic acid synthase. Unlike the bone marrow, in the liver, the defect appears to be at the level of the second enzyme d-aminolevulinic acid dehydratase. The present communication describes experiments indicating the existence of a defect in heme synthesis in the vitamin E-deficient rat. The results presented here show that vitamin E deficiency leads to a decrease in the ability of the bone marrow to synthesize &aminolevulinic acid. The locus of the defect in the liver seems to be at the step involving the formation of porphobilinogen
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