An enzymatic protective mechanism against lipid peroxidation damage to lungs of ozone-exposed rats.

Abstract

AbstractThe effects of whole animal exposure to ozone and of dietary α‐tocopherol on the occurrence in rat lung of lipid peroxidation and alteration of the activity of enzymes important in detoxification of lipid peroxides were studied. Exposure to 0.7 and 0.8 ppm ozone continuously for 5 and 7 days, respectively, significantly elevated the concentration of TBA reactants, primarily malonaldehyde, produced by lipid peroxidation, as well as the activities of glutathione (GSH) peroxidase, GSH reductase and glucose‐6‐phosphate (G‐6‐P) dehydrogenase. As a logarithmic function of dietary α‐tocopherol (0, 10.5, 45, 150 and 1500 mg/kg), the increase in formation of malonaldehyde and the increase in activities of GSH peroxidase and G‐6‐P dehydrogenase were partially inhibited. The activity of GSH reductase was not affected by dietary α‐tocopherol. The concentration of malonaldehyde and the activity of GSH peroxidase in lung were linearly correlated (p<0.001). This study confirmed the occurrence of lipid peroxidation in the lung during ozone exposure and revealed an enzymatic mechanism against damage. An apparent compensation mechanism is that with increased lipid peroxides there is increased activity of GSH peroxidase, which in turn increases lipid peroxide catabolism. The increased activities of GSH reductase and G‐6‐P dehydrogenase also function in the protective chain by providing increased levels of GSH and NADPH, respectively.