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An acute systemic acidosis in vitamin D depleted rats that was induced by ammonium chlroide feeding resulted in defective biological hydroxylation of 25-hydroxycholecalciferol to 1,25-dihydroxycholecalciferol. Impaired enzymatic hydroxylation occurred despite the presence of either hypophosphatemia or hypocalcemia. The data suggest that acidosis interfers with the adaptive enzymatic control of 25-hydroxycholecalciferol metabolism in the vitamin D depleted state.
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Lee et al. (1977) studied this question.
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