Bondy S C, Guo S X
Department of Community and Environmental Medicine, University of California, Irvine 92717-1825, USA.
Brain Res. 1996 Apr 15;716(1-2):165-70. doi: 10.1016/0006-8993(96)00008-X.
Dietary administration of ethanol to rats for 2 weeks was able to depress levels of glutathione (GSH) and Cu/Zn superoxide dismutase (SOD) in several brain regions. This was indicative of the generation of excess levels of reactive oxygen in treated animals. The potentially protective effect of both an NMDA receptor blocker (MK-801) and an internally esterified derivative of ganglioside GM1 (AGF2) upon ethanol-induced changes in these indices of oxidative stress, was studied. Both of these agents are reported to have neuroprotective properties, but neither was able to prevent ethanol-induced reduction of GSH and SOD levels in any brain area studied. In fact, both agents depressed SOD and GSH levels in midbrain independently of ethanol. MK-801 had a pronounced pro-oxidant potential, and when administered in combination with ethanol. GSH and SOD were reduced in midbrain and striatum to levels below those obtained with either agent alone. The pro-oxidant properties of ethanol may thus act independently of its actions upon the NMDA receptor. The protective properties of NMDA receptor inhibitors or gangliosides cannot be attributed to any antioxidant effect.
给大鼠喂食乙醇2周能够降低几个脑区中谷胱甘肽（GSH）和铜/锌超氧化物歧化酶（SOD）的水平。这表明在接受处理的动物中产生了过量的活性氧。研究了N-甲基-D-天冬氨酸（NMDA）受体阻滞剂（MK-801）和神经节苷脂GM1的内酯化衍生物（AGF2）对乙醇诱导的这些氧化应激指标变化的潜在保护作用。据报道，这两种药物都具有神经保护特性，但在任何研究的脑区中，它们都无法阻止乙醇诱导的GSH和SOD水平降低。事实上，这两种药物都能独立于乙醇降低中脑的SOD和GSH水平。MK-801具有明显的促氧化潜力，当与乙醇联合给药时，中脑和纹状体中的GSH和SOD水平降低到单独使用任何一种药物时所达到的水平以下。因此，乙醇的促氧化特性可能独立于其对NMDA受体的作用。NMDA受体抑制剂或神经节苷脂的保护特性不能归因于任何抗氧化作用。
