The toxic action of vitamin D is usually attributed to its effects on calcium homeostasis, as affected individuals become hypercalcaemic and develop metastatic calcified deposits in soft tissues.
However, in rats death occurs before hypercalcaemia can develop, suggesting that toxicity may be mediated by a direct effect on essential cell functions.
Whether it is 1,25-dihydroxycholcalciferol (whose plasma concentration remains essentially unchanged) or 25-hydroxy vitamin D (whose concentration may be elevated 20-fold) which is responsible for the toxic effect, is not clear.
Reference
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