Effect of model trauma on the turnover of protein and hemoprotein components of hepatic microsomal membrane in immature rats.

Administration of 14C-leucine and delta-[3,5-3H]-aminolevulinic acid to immature male rats leads to the incorporation of radioactivity into microsomal protein, including the hemoprotein cytochrome P-450. Non-hepatic regional ischemic trauma results in an increase in the half-life of total microsomal protein, but does not exert the same effect on microsomal heme-associated protein. Loss of radioactivity from microsomal hemoprotein, primarily cytochrome P-450, from traumatized animals exhibits a biphasic pattern similar to that in control animals. The half-life of both the fast-phase component and the slow-phase component is unchanged by trauma. Trauma does, however, increase the ratio of the fast- to slow-phase components of microsomal heme. A significant increase in heme oxygenase activity after trauma suggests that the fast-phase component of hepatic microsomal cytochrome P-450 is more extensively degraded.