Woods J S, Fowler B A, Eaton D L
Biochem Pharmacol. 1984 Feb 15;33(4):571-6. doi: 10.1016/0006-2952(84)90309-5.
Thallium (TlCl3) administration to rats produced a dose-dependent loss of hepatic NADPH-cytochrome c (P-450) reductase and microsomal mixed function oxidase activities within 2-4 hr following treatment. These changes occurred independently of apparent effects on microsomal heme or cytochrome P-450 content, both of which remained unchanged with respect to control levels despite transient inhibition of delta-aminolevulinic acid (ALA) synthetase and induction of heme oxygenase. These results are consistent with the recognized properties of thallium as both a flavoprotein antagonist and sulfhydryl inhibitor and differ uniquely from the action of other metals which impair mixed function oxidase activity through compromise of heme biosynthesis and heme depletion. The potential utility of thallium compounds in further evaluating the functional characteristics of NADPH-cytochrome c (P-450) reductase and its role in microsomal oxidative processes is suggested from these observations.
给大鼠施用氯化铊（TlCl3）后，在处理后的2 - 4小时内，肝脏NADPH - 细胞色素c（P - 450）还原酶和微粒体混合功能氧化酶活性出现剂量依赖性损失。这些变化独立于对微粒体血红素或细胞色素P - 450含量的明显影响而发生，尽管δ-氨基乙酰丙酸（ALA）合成酶受到短暂抑制且血红素加氧酶被诱导，但两者相对于对照水平均保持不变。这些结果与铊作为黄素蛋白拮抗剂和巯基抑制剂的公认特性一致，并且与其他通过损害血红素生物合成和血红素耗竭来损害混合功能氧化酶活性的金属的作用独特不同。从这些观察结果表明，铊化合物在进一步评估NADPH - 细胞色素c（P - 450）还原酶的功能特性及其在微粒体氧化过程中的作用方面具有潜在用途。
