Sardana M K, Drummond G S, Sassa S, Kappas A
Pharmacology. 1981;23(5):247-53. doi: 10.1159/000137557.
The administration of trivalent arsenic, either as sodium arsenite or as the trypanocidal drug melarsoprol, to rats produced a profound induction of microsomal heme oxygenase (EC 1.14.99.3) in both liver and kidney and a concomitant decrease in cytochrome P-450 content. In addition, perturbations of delta-aminolevulinate synthase were observed which showed an initial decline followed by a rebound increase in the activity of this enzyme with arsenical treatment. Pentavalent arsenic did not induce hepatic heme oxygenase but did induce the enzyme in kidney, although to a lesser extent (50%) than trivalent arsenic. Treatment of isolated chick embryo liver cells in vitro with sodium arsenite or the parasiticidal drug melarsoprol also showed a potent induction of heme oxygenase. These findings describe a new and potent ability of arsenic and parasiticidal arsenicals to induce heme oxygenase resulting in enhanced degradation of cellular heme.
给大鼠施用三价砷，无论是亚砷酸钠还是杀锥虫药物美拉胂醇，都会在肝脏和肾脏中显著诱导微粒体血红素加氧酶（EC 1.14.99.3），并伴随细胞色素P-450含量的降低。此外，还观察到δ-氨基乙酰丙酸合酶的扰动，在砷处理后，该酶的活性最初下降，随后出现反弹增加。五价砷不会诱导肝脏中的血红素加氧酶，但会诱导肾脏中的该酶，不过诱导程度比三价砷小（50%）。用亚砷酸钠或杀寄生虫药物美拉胂醇体外处理分离的鸡胚肝细胞，也显示出血红素加氧酶的强力诱导。这些发现描述了砷和杀寄生虫砷化物诱导血红素加氧酶的一种新的强大能力，导致细胞血红素降解增强。
