The Journal of Nutrition Vol. 127 No. 2 February 1997, pp. 202-209
Copyright ©1997 by the American Society for Nutritional Sciences

Fetal Exposure to Low Protein Maternal Diet Alters the Susceptibility of Young Adult Rats to Sulfur Dioxide-Induced Lung Injury

Manuscript received 20 November 1995. Initial reviews completed 26 February 1996. Revision accepted 23 September 1996.

Department of Human Nutrition, University of Southampton, Southampton, UK

The maternal diet is an important determinant of glutathione-related metabolism in rats. Glutathione (GSH) may play a major role in the detoxification of sulfur dioxide (SO₂) within the lungs. The effects of fetal 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 were housed in either room air or 286 µg SO₂/m³ for 5 h/d during a 28-d period. At the end of the final SO₂ treatment period, the rats exposed to 90 or 60 g casein/kg diets in utero exhibited significantly greater pulmonary injury, as assessed by bronchoalveolar lavage, than did those exposed to control diet in utero. Significant maternal diet-induced differences in activities of enzymes of the -glutamyl cycle were noted in the lungs and livers of rats which had not undergone SO₂ treatment. Furthermore, the response of these enzyme activities to SO₂ treatment was determined by prior exposure to the maternal diet. SO₂-treated rats exposed to control diet (180 g casein/kg) and low protein 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 treated with SO₂, of enzymes which maintain tissue GSH status either through synthesis or recycling. Differences in susceptibility to SO₂-induced tissue injury may be related to programming of GSH metabolism by the maternal diet. Alternatively, impaired immune and acute phase responses to an inflammatory insult may account for a failure to resolve initial SO₂-induced injury in rats exposed to low protein maternal diets.

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