Khan S, Rahimtula A D
Can J Physiol Pharmacol. 1987 Jan;65(1):75-9. doi: 10.1139/y87-014.
Administration of Prudhoe Bay crude oil (PBCO) to rats resulted in a dose-related increase in liver weight; rapid and marked increase in the activity of hepatic delta-aminolevulinate synthetase, the initial and rate-limiting enzyme in the heme biosynthetic pathway; rapid decline in the activity of hepatic heme oxygenase, the rate-limiting enzyme of heme catabolism; and more gradual increase in the levels of hepatic cytochrome P-450 and some mixed-function oxidase activities such as benzo[a]pyrene hydroxylase and 7-ethoxyresorufin-O-deethylase. PBCO treatment also increased renal cytochrome P-450 levels and mixed-function oxidase activities; however, delta-aminolevulinate synthetase and heme oxygenase activities were unchanged. This suggests that different regulatory mechanism(s) may be involved in renal heme metabolism and induction of monoxygenase system.
给大鼠施用普拉德霍湾原油（PBCO）会导致肝脏重量呈剂量相关增加；血红素生物合成途径中的初始限速酶——肝脏δ-氨基-γ-酮戊酸合成酶的活性迅速且显著增加；血红素分解代谢的限速酶——肝脏血红素加氧酶的活性迅速下降；以及肝脏细胞色素P-450水平和一些混合功能氧化酶活性（如苯并[a]芘羟化酶和7-乙氧基异吩恶唑酮-O-脱乙基酶）更逐渐增加。PBCO处理还会增加肾脏细胞色素P-450水平和混合功能氧化酶活性；然而，δ-氨基-γ-酮戊酸合成酶和血红素加氧酶活性未发生变化。这表明不同的调节机制可能参与了肾脏血红素代谢和单加氧酶系统的诱导。
