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Homocysteine Metabolism in Scurvy, Growth and Arteriosclerosis

Nature volume 231, pages 391–392 (1971)Cite this article

Abstract

THE connexion between the oxidative and reductive properties of ascorbic acid and the metabolic and pathological abnormalities of the connective tissues in the disease known as scurvy has yet to be explained. Decreased synthesis of chondroitin sulphate has been found in scorbutic cartilage1, and increased sulphation of proteoglycan fibrils results from increased synthesis of homocysteine in cultures of cells deficient in cystathionine synthetase2. These observations, together with that of rapid non-enzymatic reduction of dehydroascorbic acid by homocysteine3, suggested that ascorbic acid catalyses the oxidation of homocysteine in vivo, and that homocysteic acid is a precursor of the esterified sulphate of connective tissue proteoglycans.

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Authors and Affiliations

  1. James Homer Wright Pathology Laboratories, Massachusetts General Hospital, and Department of Pathology, Harvard Medical School, Boston, Massachusetts, 02115

    KILMER S. McCULLY

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  1. KILMER S. McCULLY
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McCULLY, K. Homocysteine Metabolism in Scurvy, Growth and Arteriosclerosis. Nature 231, 391–392 (1971). https://doi.org/10.1038/231391a0

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