Department of Internal Medicine, University of Texas Health Science Center at Houston, Houston, TX 77030, USA.
J Inorg Biochem. 2011 Mar;105(3):366-74. doi: 10.1016/j.jinorgbio.2010.11.012. Epub 2010 Nov 27.
Cyclooxygenase catalysis by prostaglandin H synthase (PGHS)-1 and -2 involves reaction of a peroxide-induced Tyr385 radical with arachidonic acid (AA) to form an AA radical that reacts with O(2). The potential for isomeric AA radicals and formation of an alternate tyrosyl radical at Tyr504 complicate analysis of radical intermediates. We compared the EPR spectra of PGHS-1 and -2 reacted with peroxide and AA or specifically deuterated AA in anaerobic, single-turnover experiments. With peroxide-treated PGHS-2, the carbon-centered radical observed after AA addition was consistently a pentadienyl radical; a variable wide-singlet (WS) contribution from mixture of Tyr385 and Tyr504 radicals was also present. Analogous reactions with PGHS-1 produced EPR signals consistent with varying proportions of pentadienyl and tyrosyl radicals, and two additional EPR signals. One, insensitive to oxygen exposure, is the narrow singlet tyrosyl radical with clear hyperfine features found previously in inhibitor-pretreated PGHS-1. The second type of EPR signal is a narrow singlet lacking detailed hyperfine features that disappeared upon oxygen exposure. This signal was previously ascribed to an allyl radical, but high field EPR analysis indicated that ~90% of the signal originates from a novel tyrosyl radical, with a small contribution from a carbon-centered species. The radical kinetics could be resolved by global analysis of EPR spectra of samples trapped at various times during anaerobic reaction of PGHS-1 with a mixture of peroxide and AA. The improved understanding of the dynamics of AA and tyrosyl radicals in PGHS-1 and -2 will be useful for elucidating details of the cyclooxygenase mechanism, particularly the H-transfer between tyrosyl radical and AA.
前列腺素 H 合酶(PGHS)-1 和 -2 通过环加氧酶催化,涉及过氧化物诱导的 Tyr385 自由基与花生四烯酸(AA)的反应,形成与 O(2)反应的 AA 自由基。AA 自由基的异构和 Tyr504 上形成替代的酪氨酸自由基的可能性使自由基中间体的分析变得复杂。我们比较了在厌氧、单轮实验中用过氧化物和 AA 或特定氘代 AA 处理的 PGHS-1 和 -2 的 EPR 光谱。用过氧化物处理的 PGHS-2 ,在添加 AA 后观察到的碳中心自由基始终是戊二烯基自由基; 来自 Tyr385 和 Tyr504 自由基混合物的可变宽单峰 (WS) 贡献也存在。用 PGHS-1 进行类似的反应产生的 EPR 信号与戊二烯基和酪氨酸自由基的不同比例以及另外两个 EPR 信号一致。一个对氧气暴露不敏感,是以前在抑制剂预处理的 PGHS-1 中发现的具有清晰超精细特征的窄单峰酪氨酸自由基。第二种类型的 EPR 信号是一种缺乏详细超精细特征的窄单峰信号,在暴露于氧气时消失。该信号以前归因于烯丙基自由基,但高场 EPR 分析表明,信号的~90%来自一种新型酪氨酸自由基,一小部分来自碳中心物质。通过对 PGHS-1 与过氧化物和 AA 的混合物在厌氧反应过程中不同时间捕获的样品的 EPR 光谱进行全局分析,可以解析自由基动力学。对 PGHS-1 和 -2 中 AA 和酪氨酸自由基动力学的深入了解将有助于阐明环加氧酶机制的细节,特别是 Tyr 自由基和 AA 之间的 H 转移。