Abstract
Significant numbers of South African male Bantu develop a scurvy-type skin, which appears after prolonged presence of hemosiderosis. This hemosiderosis is caused by a severe dietary iron overload. Ascorbic acid administered to the patients does not appear in the urine. Four patients with diagnosed hemosiderosis and scurvy were given 18–27-mg doses of ascorbic acid-1- 14C per os. In 24 hr as much as 47% of a dose was excreted in 14CO 2 and 20% in the urine, which accounted for a total of 67%. During a 168-hr period, the CO 2 and urine accounted for totals as high as 73% of the dose. Oxalic acid obtained from the first and second 24-hr urines contained 1% and 0.2% of the dose, respectively. The serum levels peaked at 2–4 hr after the dose. The data suggest that two rapid decarboxylation reactions, which were not related to rates of absorption occurred in these patients. Very small amounts of oxalate were formed by the splitting of the chain in the two positions to form glyoxylic acid, a precursor of oxalic acid. Six unidentified labeled components were found on autoradiographs of chromatograms of urine fractions.
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