Rickets strontium-induced

Calcidiol la-hydroxylase is not restricted to the kidney, but is also found in placenta, bone cells (in culture), mammary glands, and keratinocytes. The placental enzyme makes a significant contribution to fetal calcitriol, but it is not clear whether the calcidiol 1-hydroxylase activity of other tissues is physiologically significant or not. Acutely nephrectomized animals given a single dose of calcidiol do not form any detectable calcitriol, but there is some formation of calcitriol in anephric patients, which increases on the administration of cholecalciferol or calcidiol. However, thus extrarenal synthesis is not adequate to meet requirements, so that osteomalacia develops in renal failure (Section 3.4.1). The enzyme is inhibited, or possibly repressed, by strontium ions this is the basis of strontium-induced vitamin D-resistant rickets, which responds to the administration of calcitriol or la-hydroxycalciol, but not calciferol or calcidiol (Omdahl and DeLuca, 1971). 

Omdahl JL and DeLuca HF (1971) Strontium induced rickets metabolic basis. Science 174, 949-51. 

Reinholt FP, Hjerpe A, Jansson K, et al. 1984. Stereological studies on the epiphyseal growth plate in strontium-induced rickets. J Bone Jt Surg Am 66-A(8) 1274-1280. 

It is well known that strontium brings about a vitamin D-resistant rickets and markedly reduces intestinal calcium absorption It is now clear that the feeding of strontium represses the renal 25-OH-D3-la-hydroxylase and that the administration of 1,25-(0H)2D3 to strontium-fed animals will restore their ability to absorb calcium Thus at least in part the metabolic basis for strontium-induced rickets has been solved. Recent results suggest that strontium suppresses the 1-hydroxylase by suppressing parathyroid secretion ... 

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