Pompella A, Casini A F
Boll Soc Ital Biol Sper. 1984 Dec 30;60(12):2377-82.
Intoxication of NMRI Albino mice with bromobenzene is often followed by the appearance of neurological symptoms. The possibility was investigated that the intoxication results in glutathione (GSH) depletion in central nervous systems as seen in other tissues, and that such a depletion is followed by the development of lipid peroxidation. 18-20 hours after bromobenzene administration (15 mmoles/Kg, p.o.) GSH content of prosencephalic and metencephalic regions was depleted by 39 and 55%, respectively. Lipid peroxidation (measured by the tissue content of malonildialdehyde) was observed only when GSH content reached a threshold value, which was different for prosencephalon as compared to metencephalon (2-1.5 mumoles GSH/g and 1.2-0.7 mumoles GSH/g, respectively). Possible mechanisms underlying the phenomenon are discussed.
NMRI白化小鼠用溴苯中毒后常出现神经症状。研究了这种中毒是否会像在其他组织中那样导致中枢神经系统中的谷胱甘肽（GSH）耗竭，以及这种耗竭是否会随后引发脂质过氧化。在给予溴苯（15毫摩尔/千克，口服）18 - 20小时后，前脑和后脑区域的GSH含量分别减少了39%和55%。仅当GSH含量达到阈值时才观察到脂质过氧化（通过丙二醛的组织含量来测量），前脑和后脑的阈值不同（分别为2 - 1.5微摩尔GSH/克和1.2 - 0.7微摩尔GSH/克）。讨论了该现象背后可能的机制。
