EVIDENCE FOR ALTERED STRUCTURE AND IMPAIRED MITOCHONDRIAL ELECTRON-TRANSPORT FUNCTION IN SELENIUM DEFICIENCY

Selenium (Se) deficiency in the experimental models, Coturnix coturnix japonica and Corcyra cephalonica, resulted in impaired mitochondrial substrate oxidations and lowered thiol levels. Studies with respirator y inhibitors confirmed reduced mitochondrial electron transport enzyme activities, especially at cytochrome c oxidase (COX), the terminal se gment. Enhanced mitochondrial lipid peroxidation in Se deficiency was more pronounced in the heart tissue of the quail compared to other tis sues. Glutathione peroxidase (GSH-Px) activity toward H2O2 and cumene hydroperoxide were generally low in the insect muscle tissue and activ ity toward H2O2 was maximal in the quail heart mitochondria that was n ot very sensitive to Se status. Lowered COX activity in Se deficiency was more directly correlated with the increased level of lipid peroxid ation than with the GSH-Px activity measured, suggestive of Se mediate d protective mechanisms independent of GSH-Px. Electron microscopic ob servations revealed structural changes such as loss of cristae with pr oliferative and degenerative changes of the mitochondria in Se deficie ncy. Involvement of Se in maintaining structure and functional efficie ncy of mitochondria is evident from the present study.