Abstract
THE health hazard of ozone, the principal oxidant air pollutant of photochemical smog, has been well documented1–3. One of the notable features of ozone toxioity is the development of tolerance. When animals are exposed to a single sublethal dose of ozone they become resistant to subsequent lethal exposure. This tolerance phenomenon has been demonstrated in several species, and the effect has been shown to persist for well over one month3–6. One of its toxic effects has been attributed to its oxidative nature, and, more specifically, the initiation of lipid peroxidation7–9. Glutathione peroxidase (GP), which uses the reducing equivalent of reduced glutathione (GSH) to catalyse the decomposition of toxic hydroperoxides, and metabolically related enzymes glutathione reductase (GR) and glucose-6-phosphate dehydrogenase (G6PD), have been suggested as a key mechanism for protection of cellular components from deleterious effects of hydroperoxides10,11. The activities of these enzymes have been found to increase in the lungs of rats exposed to chronic levels of ozone9, and in tissues of rats subjected to other oxidative stress12,13. Thus changes in the activities of these enzymes seem to be related in some way to the defence mechanism against peroxidative damage. In this study, rats tolerant to ozone maintained higher activities of GP, GR and G6PD, and higher levels of GSH in the lungs following excessive exposure. The adaptive response of this potentially protective enzymic system in the lungs of ozone-tolerant rats may therefore be partly responsible for their resistance against lethal exposure.
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CHOW, C. Biochemical responses in lungs of ozone-tolerant rats. Nature 260, 721–722 (1976). https://doi.org/10.1038/260721a0
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DOI: https://doi.org/10.1038/260721a0
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