Millar T M, Stevens C R, Benjamin N, Eisenthal R, Harrison R, Blake D R
Department of Postgraduate Medicine, University of Bath, Claverton Down, UK.
FEBS Lett. 1998 May 8;427(2):225-8. doi: 10.1016/s0014-5793(98)00430-x.
Xanthine oxidoreductase (XOR) catalyses the reduction of the therapeutic organic nitrate, nitroglycerin (glyceryl trinitrate, GTN), as well as inorganic nitrate and nitrite, to nitric oxide (NO) under hypoxic conditions in the presence of NADH. Generation of nitric oxide is not detectable under normoxic conditions and is inhibited by the molybdenum site-specific inhibitors, oxypurinol and (-)BOF 4272. These enzymic reactions provide a mechanism for generation of NO under hypoxic conditions where nitric oxide synthase does not function, suggesting a vasodilatory role in ischaemia.
黄嘌呤氧化还原酶（XOR）在缺氧条件下，于烟酰胺腺嘌呤二核苷酸（NADH）存在时，催化治疗用有机硝酸盐硝酸甘油（三硝酸甘油酯，GTN）以及无机硝酸盐和亚硝酸盐还原为一氧化氮（NO）。在常氧条件下无法检测到一氧化氮的生成，且该反应受到钼位点特异性抑制剂氧嘌呤醇和（-）BOF 4272的抑制。这些酶促反应为在一氧化氮合酶不起作用的缺氧条件下生成NO提供了一种机制，提示其在缺血中具有血管舒张作用。
