Abstract

The effects of intraperitoneal injections of aluminum chloride were tested on the intestinal calcium absorption and bone calcium mobilization responses to vitamin D3 and 1,25(OH)2D3, as measured by bioassay in chicks. Aluminum at 5 mg/kg given 5 days before the bioassay in vitamin D-deficient chicks, partially blocked the intestinal calcium absorption response to low (0.65 and 3.2 nmol), but not to higher (32 nmol) doses of vitamin D3. The responses to all doses (0.32-2.1 nmol) of 1,25(OH)2D3 were partially blocked by aluminum treatment. Serum calcium values were elevated in vitamin D-deficient chicks by aluminum administration, but no consistent effects of the treatment on bone calcium mobilization in response to vitamin D3 or 1,25(OH)2D3 were noted. Aluminum treatment in vivo led to decreased 25-OH-D3-1-hydroxylase activity subsequently measured in renal homogenates; under a variety of conditions, no direct effect of aluminum on 25-OH-D3 metabolism by primary cultures of chick kidney cells was observed. The results suggest that the ability of the intestine to respond normally to 1,25(OH)2D3 may be compromised by exposure to high levels of aluminum and that the effect of this element on 25-OH-D3 metabolism observed in vivo may not be exerted by direct action on the renal cell.

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