Hyperbaric hyperoxia exaggerates respiratory membrane defects in the copper-deficient rat lung

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Abstract
Scanning (SEM) and transmission electron microscopy (TEM) were used to examine the effect of dietary copper deficiency and hyperbaric hyperoxia, alone and in combination, on lung structure. Male, weanling Sprague-Dawley† rats were fed a copper-deficient (CuD, 0.2 μg/g) or copper-adequate diet (CuA, 5.1 μg/g). After 35–41 d on their respective diets, rats from each group were placed inside a pressure vessel kept at 27°C under one of two pressure protcols. Air controls were maintained at 1 atm for 75 min. Rats exposed to oxygen were maintained at 1 atm of air plus 3 atm of oxygen for 1 h and then decompressed for 15 min. Under SEM, none of the treated lungs (CuD, CuA-O2 exposed, or CuD-O2 exposed) showed abnormal lung morphology from the conducting bronchioles down to the alveoli. Copper-deficient red blood cells were abnormally shaped. Under TEM, CuA-O2-exposed lungs showed thicker respiratory membranes, especially basement membranes and endothelial cells, and alveolar Type II cells having more than the usual number of surfactant vacuoles. CuD lungs also showed thicker endothelial and basement membrane components of the respiratory membrane, but normal looking Type II cells. CuD-O2-exposed lungs showed greatly thickened respiratory membranes and severe disruption of both endothelium and basement membrane and, judging by the increased number of nuclei per field, an increase in the number of both Type I and Type II cells. We conclude that copper deficiency enhances the damage caused by O2 toxicity, an effect that may be caused by reduced antioxidant status.

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