Accelerated accumulation of aluminum by osteoid matrix in vitamin D deficiency. An animal model of aluminum toxicity.

Abstract

To investigate the possibility that aluminum (Al) salts might associate specifically with osteoid matrix in bone, an animal model was developed in which hyperosteoidosis was controlled independently by the vitamin D status. Nonuremic rats were weaned on a vitamin D-free diet (D-) and half were given intraperitoneal AlCl3 (9.25 mg Al over 33 days). At sacrifice, serum calcium was significantly higher in Al-treated D- rats compared to D- controls (9.4 +/- 0.3 vs. 6.9 +/- 0.8 mg/dl, p less than 0.01). Serum and bone Al content were measured by flameless atomic absorption spectroscopy; Al content was 318 +/- 38 micrograms/l in serum, and 248 +/- 11 mg/kg dry bone weight in Al-treated rats, compared to almost undetectable levels in D- controls. Al was identified histochemically in Al-treated rats by its heavy deposition in subepiphyseal trabecular bone; where it occupied almost 50% of the linear trabecular bone surface, usually sandwiched between bone and osteoid seams. Both groups of animals had severe osteomalacia, but there was no evidence that Al induced a more severe lesion in addition to vitamin D deficiency. Parenteral Al was also given to rats fed a similar diet, but supplemented with vitamin D3 (D+) (cumulative dose of Al, 37.25 mg over 70 days). At sacrifice, serum Al was 671 +/- 50 micrograms/l, but bone Al was only 142 +/- 10 mg/kg, significantly less than bone Al in D- Al-treated rats. There was no evidence of osteomalacia in D+ Al-treated rats in which histochemical staining for Al was essentially negative.(ABSTRACT TRUNCATED AT 250 WORDS)