Willmore L J, Rubin J J
Brain Res. 1984 Apr 2;296(2):389-92. doi: 10.1016/0006-8993(84)90080-5.
Addition of iron salts to suspensions of subcellular organelles or polyunsaturated fatty acids results in the formation of oxidative free radicals with subsequent initiation of lipid peroxidation. Pretreatment of rats with anti-oxidants prevents peroxidation following isocortical ferrous chloride injection, and increases the rate of resolution of iron-induced focal edema. In this experiment, treatment of rats at the time of injection of 5 microliters of 100 mM FeCl2 with tocopherol and DMSO caused decreased formation of brain peroxidation at the injection site, as measured by formation of MDA. Tocopherol failed to change the quantity of tissue fluid accumulation. However, DMSO alone, or combined with tocopherol, hastened the resolution of brain edema. Tocopherol may terminate peroxidation reactions by donation of a phenolic hydrogen, forming a quinone of tocopherol. DMSO has many pharmacologic effects; however, inhibition of initiation reactions by scavenging hydroxyl radicals, and direct and indirect effects on focal edema accumulation may account for our observations.
向亚细胞器或多不饱和脂肪酸悬浮液中添加铁盐会导致氧化自由基的形成,并随后引发脂质过氧化。用抗氧化剂对大鼠进行预处理可防止在注射异皮质氯化亚铁后发生过氧化,并提高铁诱导的局灶性水肿的消退速度。在本实验中,在注射5微升100 mM FeCl2时用生育酚和二甲基亚砜处理大鼠,通过丙二醛的形成来衡量,注射部位的脑过氧化形成减少。生育酚未能改变组织液积聚的量。然而,单独的二甲基亚砜或与生育酚联合使用,都加速了脑水肿的消退。生育酚可能通过提供一个酚羟基氢来终止过氧化反应,形成生育酚醌。二甲基亚砜有许多药理作用;然而,通过清除羟基自由基抑制引发反应,以及对局灶性水肿积聚的直接和间接影响可能解释了我们的观察结果。