Yu P H
Neuropsychiatry Research Unit, College of Medicine, University of Saskatchewan, Saskatoon, Canada.
J Neural Transm Suppl. 1998;52:201-16. doi: 10.1007/978-3-7091-6499-0_19.
Semicarbazide-sensitive amine oxidase (SSAO) is located in the vascular smooth muscles, retina, kidney and the cartilage tissues, and it circulates in the blood. The enzyme activity has been found to be significantly increased in blood and tissues in diabetic patients and animals. Methylamine and aminoacetone are endogenous substrates for SSAO. The deaminated products are formaldehyde and methylglyoxal respectively, as well as H2O2 and ammonia, which are all potentially cytotoxic. Formaldehyde and methylglyoxal are cytotoxic towards endothelial cells. Excessive SSAO-mediated deamination may directly initiate endothelial injury and plaque formation, increase oxidative stress, which can potentiate oxidative glycation, and/or LDL oxidation and damage vascular systems. Formaldehyde is also capable of exacerbating advanced glycation, and thus increase the complexity of protein cross-linking. Uncontrolled SSAO-mediated deamination may be involved in the acceleration of the clinical complications in diabetes.
氨基脲敏感胺氧化酶（SSAO）位于血管平滑肌、视网膜、肾脏和软骨组织中，并在血液中循环。已发现糖尿病患者和动物的血液及组织中该酶活性显著增加。甲胺和氨基丙酮是SSAO的内源性底物。脱氨产物分别是甲醛和甲基乙二醛，以及过氧化氢和氨，它们都具有潜在的细胞毒性。甲醛和甲基乙二醛对内皮细胞具有细胞毒性。过量的SSAO介导的脱氨作用可能直接引发内皮损伤和斑块形成，增加氧化应激，从而增强氧化糖基化作用，和/或低密度脂蛋白氧化并损害血管系统。甲醛还能够加剧晚期糖基化，从而增加蛋白质交联的复杂性。不受控制的SSAO介导的脱氨作用可能参与糖尿病临床并发症的加速发展。
