Department of Physiology and Pharmacology, West Virginia University, Morgantown, WV, USA.
Adv Exp Med Biol. 2019;1127:59-65. doi: 10.1007/978-3-030-11488-6_4.
Inhibition of xanthine oxidoreductase (XOR) has proven beneficial in a plethora of inflammatory disease processes due to a net reduction in pro-inflammatory oxidants and secondary nitrating species. Electrophilic nitrated fatty acid derivatives, such as nitro-oleic acid (OA-NO) are also noted to display a broad spectrum of anti-inflammatory effects via interaction with critical signaling pathways. An alternative process in which nitrated fatty acids may extend anti-inflammatory actions is via inactivation of XOR, a process that is more effective than allo/oxypurinol-mediated inhibition. Herein, we describe the molecular aspects of nitrated fatty acid-associated inactivation of XOR, identify specificity via structure function relationships and discuss XOR as a crucial component of the anti-inflammatory portfolio of nitrated fatty acids.
黄嘌呤氧化酶(XOR)的抑制作用已被证明在多种炎症性疾病过程中是有益的,因为它可以减少促炎氧化剂和次级硝化物质的产生。亲电子硝化脂肪酸衍生物,如硝基油酸(OA-NO),也被认为通过与关键信号通路相互作用,具有广泛的抗炎作用。硝化脂肪酸延长抗炎作用的另一种方式是通过灭活 XOR,这种方式比 allo/氧嘌呤醇介导的抑制更为有效。本文描述了与硝化脂肪酸相关的 XOR 失活的分子机制,通过结构-功能关系确定了特异性,并讨论了 XOR 作为硝化脂肪酸抗炎作用的关键组成部分。