Deficiencies in antioxidant defense mechanisms within the lungs of premature infants are generally accepted as predisposing to the development of bronchopulmonary dysplasia (BPD). Pharmacological management of premature infants often utilizes the glucocorticoid, dexamethasone. Investigators have shown, however, that DEX accelerates hyperoxia-induced lung injury, a critical factor in the development of BPD. The purpose of this study was to determine the effect of DEX and hyperoxia on the critical intracellular antioxidant GSH. We administered 1 mg/kg DEX or vehicle ip and immediately placed rats in>95% O2. At 0, 24, and 48 h of hyperoxia-exposure, lung, liver and plasma GSH, as well as lung and liver glutathione disulfide (GSSG) were measured. The data were analyzed by two way ANOVA to determine the effect of DEX and hyperoxia, and a modified t test when appropriate. Lung GSH increased in the hyperoxia-exposed rats independent of DEX treatment, while lung GSSG increased in both hyperoxia-exposed and DEX-treated rats. We found no differences in plasma GSH. The earlier increase in lung GSSG suggests that DEX increases the oxidant stress experienced by the lung, and that the possible deleterious effects of glucocorticoid treatment on the oxidant/antioxidant balance should be considered in infants exposed to hyperoxia.Table

Table 1
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