Abstract

Prolonged exposure of C57B16 mice to pure O2 at 1 ATA induced pulmonary edema associated with involution of lymphoid system and depressed immunity. The consequences of these toxic events were evaluated by 1) mortality rate, 2) determination of pulmonary water, 3) thymic and splenic cellularity, and 4) humoral (primary antibodies) and cellular (mitogenic) immune responses. Pretreatment of mice with 125 mg kg-1 of diethyldithiocarbamate (DDC) several days before exposure to O2 resulted in 1) an increase in animal survival (92-100% vs. 59% O2 controls), 2) a reduction in pulmonary edema, 3) partial stabilization of thymus and spleen lymphocyte populations, and 4) restoration of the humoral response (specific antibodies appeared earlier than in O2 control animals) and improvement of the mitogenic proliferative response of the spleen cells after hyperoxia. None of these effects were observed when DDC treatment coincided with the beginning of exposure. Our results indicated that DDC protects mice from both pulmonary and lymphoid hyperoxic injury, but only in a partial manner. It is suggested that the mechanism of this antioxidative property is indirect.