Effect of Short-Term Ischemic Trauma on the Hepatic Cytochrome P-450 Monooxygenase System in the Neonatal Rat

Abdominal aorta ligation in neonatal rats was used as a model to evaluate drug-metabolizing activities after trauma. Short-term ischemic trauma (24 h) was found to have a significant effect on hepatic microsomal cytochrome P-450 content, NADPH-cytochrome c reductase activity, and cytochrome P-450-dependent electron transport capacity. In pre-weanling animals, trauma caused a decrease in hepatic microsomal cytochrome P-450 content, but increased NADPH-cytochrome c reductase activity. The electron transport capacity of the cytochrome P-450 system is reduced in traumatized pre-weanling rats, suggesting that cytochrome P-450 may be the rate-limiting step for this enzyme system in animals of this age. After weaning, the electron transport capacity of this enzyme system is greater in traumatized animals than in control animals, indicating that a different rate-limiting factor dominates in these animals.