Toxic effects of cadmium on the developing rat lung. II. Glycogen and phospholipid metabolism

Maternal exposure to Cd reduces lung weight and alters pulmonary surfactant accumulation in the fetus. This may lead to respiratory distress and death postnatally. In this study, the effects of maternal Cd administration on additional biochemical parameters of the fetal lung were investigated. Pregnant rats were given sc injections of 8 mg/kg CdCl2 on the 12-15 of gestation and sacrificed throughout late gestation. Fetal lungs were examined for protein, DNA, and glycogen. Incorporation of choline into total and disaturated phosphatidylcholine and sphingomyelin were measured in fetal lung slices. The DNA content of the treated lungs was reduced, but the protein/DNA ratio was not altered. Thus the reduced lung weight was due to hypoplasia, not hypotrophy. Incorporation of choline into pulmonary sphingomyelin was not altered by the treatment. Choline incorporation into both total and disaturated phosphatidylcholine, the most important surfactant component, was reduced on the final days of gestation. Glycogen was reduced in both absolute quantity and cellular concentration of lungs of treated fetuses. Glucose derived from glycogen is a major metabolic substrate in the fetal lung and probably contributes greatly to phospholipid synthesis. The reduction in glucose concentration in lungs of treated fetuses may be a factor in the diminished synthesis of pulmonary surfactant phosphatidylcholine before birth. Prenatal Cd exposure (1) causes pulmonary hypoplasia, (2) reduces the amount of glycogen present in the fetal lung, and (3) diminishes the rate of synthesis of pulmonary surfactant phosphatidylcholine.