The effects of "oxygen radicals" generated in the medium on lenses in organ culture: inhibition of damage by chelated iron.
The effects of "oxygen radicals" generated in the medium on lenses in organ culture: inhibition of damage by chelated iron.
复制标题
培养基中产生的“氧自由基”对器官培养中晶状体的影响：螯合铁抑制损伤。
DOI：
10.1016/0003-9861(85)90372-8
复制
发表时间：
1985
影响因子：
3.9
通讯作者：
Reddy,VN
中科院分区：
文献类型：
--
作者：
ZiglerJr,JS;JerniganJr,HM;Garland,D;Reddy,VN
Rat lenses in organ culture were exposed to activated species of oxygen generated in the culture medium either by xanthine oxidase and hypoxanthine or by riboflavin and visible light, two systems which have been shown to produce superoxide and H2O2. In each case there was marked damage to carrier-mediated transport systems of the lens. Under standard culture conditions this damage was strongly inhibited by catalase, but not by superoxide dismutase (SOD). By the addition to the medium of chelated iron, hydroxyl radicals were produced in a Fenton reaction with a concomitant decrease in H2O2levels. With both oxygen radical-generating systems, the addition of chelated iron strongly inhibited lens damage. This inhibitory effect could be reversed by the addition of SOD with the chelated iron. Under such conditions SOD converts superoxide anion to H2O2, thereby preventing reduction of the chelated iron and thus stopping the generation of hydroxyl radicals. Increased lens damage following addition of SOD to the iron-containing systems correlated with higher H2O2concentrations, and was inhibited by catalase. These findings suggest that, when generated in the fluids surrounding the lens, H2O2poses a much greater oxidative stress for the lens than do the superoxide or hydroxyl free radicals.
