Munday R, Manns E
AgResearch, Ruakura Agricultural Research Centre, Hamilton, New Zealand.
J Appl Toxicol. 1998 Mar-Apr;18(2):161-5. doi: 10.1002/(sici)1099-1263(199803/04)18:2<161::aid-jat491>3.0.co;2-3.
Some aromatic polyamines form very stable free radicals and readily undergo autoxidation with concomitant formation of 'active oxygen' species. These substances cause necrosis of striated muscle in rats, and it has been suggested that this is due to free radical formation and disruption of energy production through their oxidation via the cytochrome c/cytochrome oxidase system of mitochondria. 2,3,6-Triaminopyridine, which is structurally related to the myotoxic amines and likewise undergoes autoxidation and disrupts mitochondrial metabolism, is a metabolite of the widely used urinary analgesic phenazopyridine. When administered to rats, triaminopyridine caused extensive necrosis of skeletal muscle and a lesser degree of damage to heart muscle. It also induced vacuolation and necrosis of distal tubules of the kidney, associated with tubular dilatation and cast formation. Both muscle damage and renal tubular necrosis have been reported following use or abuse of phenazopyridine, and it is likely that triaminopyridine is responsible for both of these effects.
一些芳香族多胺会形成非常稳定的自由基，并容易发生自氧化，同时形成“活性氧”物质。这些物质会导致大鼠横纹肌坏死，有人认为这是由于自由基的形成以及通过线粒体的细胞色素c/细胞色素氧化酶系统氧化而破坏能量产生所致。2,3,6-三氨基吡啶与具有肌毒性的胺类在结构上相关，同样会发生自氧化并破坏线粒体代谢，它是广泛使用的尿路镇痛药非那吡啶的一种代谢产物。给大鼠服用三氨基吡啶会导致骨骼肌广泛坏死，对心肌的损伤程度较轻。它还会引起肾远端小管的空泡化和坏死，并伴有肾小管扩张和管型形成。使用或滥用非那吡啶后均有肌肉损伤和肾小管坏死的报道，很可能三氨基吡啶是这两种效应的罪魁祸首。
