CHOLECALCIFEROL HYDROXYLATION IN RAT HEPATOCYTES UNDER THE INFLUENCE OF PREDNISOLONE
A. V. Khomenko
Palladin Institute of Biochemistry, National Academy of Sciences of Ukraine, Kyiv;
Glucocorticoid therapy is accompanied by development of processes typical of steroid osteoporosis. Indirect effects of glucocorticoids on the bone tissue are due to changes in mineral metabolism, which is regulated by vitamin D3. In this connection, we studied the influence of prednisolone on cholecalciferol metabolism. The study has shown that prednisolone action causes impairment of cholecalciferol metabolism in hepatocytes due to inhibiting vitamin D3 25-hydroxylase activity. Microsomal (CYP2R1) and mitochondrial (CYP27A1) isoenzymes of vitamin D3 25-hydroxylase were found to function at different concentrations of the substrate. The relative protein contents of the isoenzymes greatly differed in the liver with the prevalence of CYP27A1 over CYP2R1. Prednisolone administration resulted in the lowering of both mitochondrial and microsomal isoenzymes of vitamin D3 25-hydroxylase. The inhibition of vitamin D3 25-hydroxylating system in hepatocytes contributed to a significant reduction in blood serum 25OHD3.
Key words: vitamin D3, 25OHD3, vitamin D3 25-hydroxylase activity, CYP2R1, CYP27A1, hepatocytes, glucocorticoids, prednisolone.
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