Cadmium impact and osteoporosis: mechanism of action

Abstract

CONTEXT: Cadmium (Cd) is a widespread environmental pollutant that is associated with increased risk of osteoporosis. It has been proposed that Cd's toxic effect on bone is exerted via impaired activation of vitamin D, secondary to the kidney effects. OBJECTIVE: The present study was designed to investigate the damaging impact of Cd in drinking water on bone from biochemical and histopathological point of view. MATERIALS AND METHODS: This study was conducted on 30, 3-months-old female Sprague Dawley rats exposed to cadmium chloride in a dose of 50 mg Cd/L in drinking water for 3 months. Serum was taken for determination of calcium, phosphorous levels, parathyroid hormone, 1,25 dihydroxy vitamin D(3), osteocalcin (OC) and bone specific alkaline phosphatase (BALP) activity. RESULTS: The result revealed that Cd administration induces significant increase in serum calcium (Ca), phosphorous (P) and parathyroid hormone (PTH) levels in concomitant with significant reduction in serum vitamin D(3), osteocalcin (OC) levels and bone specific alkaline phosphatase (BALP) activity. CONCLUSION: The present study provided clear evidence that long-term exposure to cadmium chloride produced marked abnormalities in bone biomarkers and increasing risk of fracture.