FETAL EXPOSURE TO LOW-PROTEIN MATERNAL DIET ALTERS THE SUSCEPTIBILITYOF YOUNG-ADULT RATS TO SULFUR DIOXIDE-INDUCED LUNG INJURY

The maternal diet is an important determinant of glutathione-related m etabolism in rats. Glutathione (GSH) may play a major role in the deto xification of sulfur dioxide (SO2) within the lungs. The effects of fe tal exposure to a low protein maternal diet upon later susceptibility to pulmonary injury induced by chronic SO2 exposure were evaluated in young adult rats. Pregnant rats were fed purified diets containing 180 g casein/kg (control diet) or 120, 90 or 60 g casein/kg (experimental diets). After parturition, all dams were fed a standard non-purified diet (189 g protein/kg diet). The pups thus differed only in terms of protein nutrition during gestation. At seven wk of age the male pups w ere housed in either room air or 286 mu g SO2/m(3) for 5 h/d during a 28-d period. At the end of the final SO2 treatment period, the rats ex posed to 90 or 60 g casein/kg diets in utero exhibited significantly g reater pulmonary injury, as assessed by bronchoalveolar lavage, than d id those exposed to control diet in utero. Significant maternal diet-i nduced differences in activities of enzymes of the gamma-glutamyl cycl e were noted in the lungs and livers of rats which had not undergone S O2 treatment. Furthermore, the response of these enzyme activities to SO2 treatment was determined by prior exposure to the maternal diet. S O2-treated rats exposed to control diet (180 g casein/kg) and low prot ein diet (60 g casein/kg), but not those exposed to 120 or 90 g casein /kg diets, tended to augment the activities, relative to rats not trea ted with SO2, of enzymes which maintain tissue GSH status either throu gh synthesis or recycling, Differences in susceptibility to SO2-induce d tissue injury may be related to programming of GSH metabolism by the maternal diet. Alternatively, impaired immune and acute phase respons es to an inflammatory insult may account for a failure to resolve init ial SO2-induced injury in rats exposed to low protein maternal diets.