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Proof of the curative action of vitamin D for rickets was established by the studies of many investigators (1, 2). It is now known that therapeutic doses of this vitamin bring about increased calcium absorption from the intestinal tract (3), while massive doses induce hypercalcemia (4) and, experimentally at least, a combination of skeletal resorption and vigorous bone-matrix formation (5-7). Also, in the hypoparathyroid individual, administration of vitamin D results in an increased excretion of phosphorus and usually of calcium (8, 9). Knowledge of the biochemical or enzymatic means by which vitamin D induces the foregoing effects would greatly enhance our understanding of mineral and bone metabolism. An approach to the study of this problem was afforded by the reports of Warkany and his co-workers (10-12) on bioassays of vitamin D in sera of animals and humans. Vitamin D in aqueous solution, however, is known to be readily oxidized and thereby rendered inactive (13). This suggests that the vitamin, as it exists in serum, is in some manner protected and may not be in a free or unaltered state. Therefore, in our initial studies on vitamin

the journal of clinical investigation/the journal of clinical investigation

STUDIES OF ANTIRICKETIC ACTIVITY IN SERA FROM PATIENTS WITH DISORDERS OF CALCIUM METABOLISM AND PRELIMINARY OBSERVATIONS ON THE MODE OF TRANSPORT OF VITAMIN D IN HUMAN SERUM*