Slivka A, Cohen G
Department of Neurology, Mount Sinai School of Medicine, New York, NY 10029.
Brain Res. 1993 Apr 9;608(1):33-7. doi: 10.1016/0006-8993(93)90770-n.
The mechanisms underlying cell damage in stroke or during experimental brain ischemia are not fully understood. L-Cysteine, an excitotoxic amino acid that could contribute to tissue damage, is normally found in relatively low levels in brain (ca. 0.05 mumol/g), compared to the cysteine-containing tripeptide, glutathione (GSH, ca. 1.5 mumol/g). We have observed that during brain ischemia in gerbils, levels of cysteine rise 10-13-fold over an 8 h period to 0.66 and 0.62 mumol/g, respectively, in the ischemic hippocampus and striatum. At the same time, levels of GSH fall by 0.84 and 0.94 mumol/g, respectively. The elevated free cysteine may be derived largely from GSH. The levels of cysteine found in ischemic brain are similar to those reported after parenteral administration of neurotoxic doses of L-cysteine to perinatal rats. The remarkable increase in cysteine during brain ischemia, coupled to its neurotoxic properties, may play a role in aspects of brain damage during or following brain ischemia.
中风或实验性脑缺血期间细胞损伤的潜在机制尚未完全明确。L-半胱氨酸是一种可能导致组织损伤的兴奋性毒性氨基酸，与含半胱氨酸的三肽谷胱甘肽（GSH，约1.5 μmol/g）相比，其在脑内的正常水平相对较低（约0.05 μmol/g）。我们观察到，在沙鼠脑缺血期间，半胱氨酸水平在8小时内分别在缺血海马体和纹状体中升高10至13倍，达到0.66和0.62 μmol/g。与此同时，GSH水平分别下降0.84和0.94 μmol/g。升高的游离半胱氨酸可能主要来源于GSH。缺血脑中发现的半胱氨酸水平与给围产期大鼠肠胃外注射神经毒性剂量的L-半胱氨酸后所报告的水平相似。脑缺血期间半胱氨酸的显著增加，加上其神经毒性特性，可能在脑缺血期间或之后的脑损伤方面发挥作用。
