Abstract
Swiss Webster mice were continously exposed to an atmosphere containing 1.5 ppm ozone (O 3) for 5 dyas. Control mice breathed filtered air. Immediately following the exposure period each mouse was then injected with [1- 14C] ascorbic acid. The rate of disappearance of [1- 14C] ascorbic acid and the levels of total ascorbic acid were determined in serum, lung, liver, and the remaining carcass over a 9-day period. O 3 exposure caused transient 3ecreases in the ascorbic acid levels in liver and serum, whereas lung ascorbic acid levels increased. The apparent biological half-life of ascorbate in carcasses (minus lung and liver) from O 3-exposed mice, was significantly prolonged. Significant changes were also observed in the net flux of ascorbic acid in all tissues examined. The results indicated that the change in ascorbic acid levels in a given tissue appeared to reflect changes in the rate of ascorbic acid degradation, its mobilization or tissue compartmentalization, rather than increased synthesis in response to O 3 exposure.
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