Effect of parathyroid hormone on antioxidant enzyme activity and lipid peroxidation of erythrocytes in five-sixths nephrectomized rats

Abstract

The purpose of the study was to investigate the effects of parathyroid hormone (PTH) infusion on antioxidant enzyme activity and lipid peroxidation of erythrocytes in five-sixths nephrectomized (Nx) rats. Five-sixths Nx rats had a higher osmotic fragility in red blood cells (RBC). Thyroparathyroidectomy (TPTX) effectively decreased the abnormality of osmotic fragility in RBC in Nx rats. PTH infusion in Nx-TPTX rats markedly increased the osmotic fragility in RBC. Total glutathione was measured by using the enzyme-recycling method. We found elevated glutathione levels in RBC of five-sixths Nx rats, but this elevation could be inhibited by TPTX and recovered by PTH infusion in Nx-TPTX rats. Five-sixths Nx rats had a lower glutathione peroxidase activity in RBC, but TPTX or PTH infusion was not found to alter the decrease of the glutathione peroxidase activity in RBC of five-sixths Nx rats. These rats had a higher activity in RBC superoxide dismutase as compared with sham-operated controls (p < 0.05), but the higher activity in RBC superoxide dismutase in Nx rats had been inhibited by TPTX. PTH infusion recovered the higher activity in RBC superoxide dismutase in five-sixths Nx-TPTX rats. Nx rats were not found to alter the activity of catalase in RBC. Neither could TPTX or PTH infusion in Nx rats influence the activity of catalase in RBC. A high lipid peroxidation in RBC was found in five-sixths Nx rats, namely, increased formation of malondialdehyde (MDA) in RBC had been induced to produce lipid peroxidation by H2O2, but neither TPTX nor PTH infusion could inhibit or enhance the increase of lipid peroxidation in RBC of Nx rats. These results indicate that PTH infusion did not increase the susceptibility to lipid peroxidation in RBC of five-sixths Nx rats. Thus, the increased osmotic fragility in RBC induced by PTH infusion may not result from the reduction in the RBC defense mechanism against free radical toxicity.