Wolff S P, Spector A
Department of Ophthalmology, College of Physicians and Surgeons, Columbia University, New York, NY 10032.
Exp Eye Res. 1987 Dec;45(6):791-803. doi: 10.1016/s0014-4835(87)80096-9.
The ability of 2,6-dimethoxyquinone (DMQ) to impair 86Rb uptake by bovine lens epithelial cells was found to be independent of exogenous ascorbate in contrast to the impairment induced by Fe/Cu or riboflavin plus light. The cytotoxicity was associated with an electron spin resonance (ESR) detectable singlet radical (g = 2.0062) which also formed on incubation of DMQ with glutathione (GSH) or gamma-crystallin in vitro. Formation of the stable free radical appeared to require conjugation of DMQ by peptidyl thiol and required transition metal catalysis. A structure for the DMQ-glutathione free radical conjugate is proposed. Redox activity of quinone conjugates is suggested to be of relevance to an oxidative damage hypothesis of cataract.
与铁/铜或核黄素加光照所诱导的损伤不同，发现2,6 - 二甲氧基醌（DMQ）损害牛晶状体上皮细胞摄取⁸⁶Rb的能力与外源性抗坏血酸无关。细胞毒性与电子自旋共振（ESR）可检测到的单线态自由基（g = 2.0062）有关，该自由基在体外将DMQ与谷胱甘肽（GSH）或γ-晶状体蛋白温育时也会形成。稳定自由基的形成似乎需要肽基硫醇对DMQ进行共轭，并且需要过渡金属催化。提出了DMQ - 谷胱甘肽自由基共轭物的结构。醌共轭物的氧化还原活性被认为与白内障的氧化损伤假说有关。
