Changes in urinary deoxypyridinoline [DPD] and serum osteocalcin levels in cadmium chloride induced liver damage in rats before and after vitamin D therapy

ABSTRACT

Chronic liver diseases have an increased prevalence of metabolic bone diseases in the form of osteopenia and osteoporosis, however, there is little information about the mechanisms of these effects. The present study was aimed to investigate the importance of changes of urinary deoxypyridinoline [Dpd] and serum osteocalcin levels in experimentally induced hepatocellular injury in rats by cadmium chloride [CdCl[2]] as well as to clarify the effect of l,25 [OH][2] D[3] administration. Thirty adult male albino rats were used. The study included 3 groups each of 10 rats, group 1 was normal rats used as a control group, group 2 consisted of rats with induced hepatic damage by CdCl[2] [0.1 mg/kg subcutaneously for 4 weeks] and group 3 consisted of rats with CdCl[2]induced damage and treated with 1,25 [OH][2] D[3] administration [0.1 micro g/kg orally once daily for one week]. Blood and urine samples were collected from all rats at the end of the experiment to measure the levels of the following parameters serum alanine and aspartate aminotransferases [ALT and AST], urinary Dpd levels as well as serum osteocalcin levels. The results of the present study showed that CdCl[2] induced a significant elevation in the mean values of ALT and AST. Urinary Dpd levels were significantly high after CdCl[2] injection. On the other hand, serum osteocalcin levels were significantly reduced especially in group 2 as compared to the other groups. The present study showed that administration of 1,25 [OH][2] D[3] to group 3 lead to reduction in levels of urinary Dpd and increased levels of serum osteocalcin but did not affect levels of serum transaminases. It was concluded that CdCl[2] induced hepatocellular injury is associated with increased bone resorption and decreased bone formation. Administration of 1.25 [OH][2] D[3] can stop these changes by preventing the progression of bone dystrophy associated with hepatocellular damage