Abstract
ABSTRACT
A possible mechanism by which chemical compounds found in industrial waste products may cause tissue injury is through potentiation of damage by free radical formation. In these studies we have used a model system of rats exposed to normobaric hyperoxia to test for effects of chemical compounds that may potentiate or change fluxes of free radicals on animal survival or lung injury, lung Superoxide dismutase, catalase, glutathione peroxidase, glucose-6-phosphate dehydrogenase and glutathione. The chemical compounds tested, including diethylmaleate (DEM), diethyldithiocarbamate (DDC), disulfiram and nitrofurantoin, all potentiated oxygen toxicity but produced their effects through different mechanisms related to changes in free radical levels. Our model system may be useful to test a variety of chemical compounds of industrial wastes for possible potentiating effects on lung injury caused by free radical generation.
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