Bondy S C, Guo S X
Department of Community and Environmental Medicine, University of California, Irvine 92715.
Eur J Pharmacol. 1994 Aug 3;270(4):349-55. doi: 10.1016/0926-6917(94)90011-6.
The effect of ethanol exposure upon several parameters relating to oxidative stress has been examined in brain and liver. A single administration of either acetaldehyde or ethanol was able to enhance rates of generation of reactive oxygen species in liver but this effect was not apparent in the cerebral cortex. Glutamine synthetase is especially sensitive to inactivation by free radicals and evidence for cumulative oxidative damage to this enzyme was found in liver and to a lesser extent in cerebral cortex. This enzyme was depressed in liver after both a single injection of acetaldehyde or ethanol, or after more extended dosing. The liver was also more susceptible than cerebral cortex, to pro-oxidant effects as judged by depression of glutathione after acute dosing with either solvent. Enzyme inhibition representing temporally summated oxidative events may be a more sensitive procedure than direct measurement of rates of formation of active oxygen species and may find especially utility in the detection of prolonged low level pro-oxidant activity.
已经在脑和肝脏中研究了乙醇暴露对与氧化应激相关的几个参数的影响。单次给予乙醛或乙醇能够提高肝脏中活性氧的产生速率，但这种效应在大脑皮层中并不明显。谷氨酰胺合成酶对自由基灭活特别敏感，在肝脏中发现了对该酶累积氧化损伤的证据，在大脑皮层中的程度较小。单次注射乙醛或乙醇后，或在更长时间给药后，该酶在肝脏中均受到抑制。急性给予任何一种溶剂后，通过谷胱甘肽的降低判断，肝脏比大脑皮层对促氧化作用更敏感。代表时间上累积氧化事件的酶抑制可能是比直接测量活性氧形成速率更敏感的方法，并且在检测长期低水平促氧化活性方面可能特别有用。
