朱本占研究员在自由基化学研究方面又取得重要进展，其有关“过氧化氢和卤代醌不依赖于金属离子存在型的羟基自由基产生分子机理”的研究发表在国际著名的综合性学术期刊美国《国家科学院院刊》（PNAS）上。
羟基自由基（HO·）被公认是生物系统中最具活性的活性氧物种，能导致生物体内DNA，蛋白质和脂质氧化损伤。目前，关于羟基自由基的产生机理，最被广泛接受的是过渡金属离子催化的Fenton反应。朱本占等曾发现五氯酚的代谢产物之一四氯苯醌与H2O2反应可产生羟基自由基，其特别之处在于此过程不依赖于金属离子的存在。但其潜在的分子机理仍不清楚。
以电子自旋共振结合二级自由基自旋捕获技术为手段，通过研究发现：四氯苯醌（TCBQ，五氯酚等环境污染物的有毒代谢产物），而不是相应的半醌负离子自由基（TCSQ·-）对羟基自由基的产生极其重要。TCBQ和H2O2反应的主要产物采用电喷雾-四极杆飞行时间质谱仪鉴定为三氯羟基-1，4-苯醌（TrCBQ-OH）的离子形式。研究还发现，反应产物TrCBQ-OH中的氧原子来自于H2O2。 基于这些数据和分析，提出以下假设：TCBQ和H2O2反应产生羟基自由基不是通过一种依赖于半醌的有机Fenton反应进行，而是通过下述机理：H2O2对TCBQ进行亲核攻击，形成一种三氯氢过氧基-1，4-苯醌（TrCBQ-OOH）中间产物，这种中间产物能均裂产生羟基自由基和三氯羟基-1,4-苯醌自由基（TrCBQ-O·）。TrCBQ-O·随后能歧化形成三氯羟基-1,4-苯醌的离子形式（TrCBQ-O-）。
上述反应途径展示了一种新型的羟基自由基产生机理：羟基自由基的形成不需要具有氧化还原活性的过渡金属离子参与，也不需要光照，辐射和高温加热。该机理能部分解释许多杀虫剂（如多氯代酚，六氯苯和橙色剂等）的致癌性，这些物质能在体内代谢成四氯，三氯，二氯和一氯苯醌。（来源：中国科学院生态环境研究中心）
生物谷推荐原始出处：
（PNAS），March 6, 2007 | vol. 104 | no. 10 | 3698-3702，Ben-Zhan Zhu, Balz Frei
Mechanism of metal-independent decomposition of organic hydroperoxides and formation of alkoxyl radicals by halogenated quinones
Ben-Zhan Zhu*,,, Hong-Tao Zhao, Balaraman Kalyanaraman, Jun Liu*, Guo-Qiang Shan*, Yu-Guo Du*, and Balz Frei
*State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center for Eco-Environmental Sciences, Chinese Academy of Sciences, Beijing 100085, People's Republic of China; Linus Pauling Institute, Oregon State University, Corvallis, OR 97331; and Biophysics Research Institute, Medical College of Wisconsin, Milwaukee, WI 53226
Edited by Jack Halpern, University of Chicago, Chicago, IL, and approved December 18, 2006 (received for review July 2, 2006)
The metal-independent decomposition of organic hydroperoxides and the formation of organic alkoxyl radicals in the absence or presence of halogenated quinones were studied with electron spin resonance (ESR) and the spin-trapping agent 5,5-dimethyl-1-pyrroline N-oxide (DMPO). We found that 2,5-dichloro-1,4-benzoquinone (DCBQ) markedly enhanced the decomposition of tert-butylhydroperoxide (t-BuOOH), leading to the formation of the DMPO adducts with t-butoxyl radicals (t-BuO) and methyl radicals (CH3). The formation of DMPO/t-BuO and DMPO/CH3 was dose-dependent with respect to both DCBQ and t-BuOOH and was not affected by iron- or copper-specific metal chelators. Comparison of the data obtained with DCBQ and t-BuOOH with those obtained in a parallel study with ferrous iron and t-BuOOH strongly suggested that t-BuO was produced by DCBQ and t-BuOOH through a metal-independent mechanism. Other halogenated quinones were also found to enhance the decomposition of t-BuOOH and other organic hydroperoxides such as cumene hydroperoxide, leading to the formation of the respective organic alkoxyl radicals in a metal-independent manner. Based on these data, we propose a mechanism for DCBQ-mediated t-BuOOH decomposition and formation of t-BuO: a nucleophilic attack of t-BuOOH on DCBQ, forming a chloro-t-butylperoxyl-1,4-benzoquinone intermediate, which decomposes homolytically to produce t-BuO. This represents a mechanism of organic alkoxyl radical formation not requiring the involvement of redox-active transition metal ions.
