Yang C S, Chen W Y, Tsai P J, Cheng F C, Kuo J S
Department of Education and Research, Taichung Veterans General Hospital, Taiwan, R.O.C.
Biochem Pharmacol. 1997 Feb 7;53(3):357-61. doi: 10.1016/s0006-2952(96)00729-0.
Glutathione (GSH), present in a high concentration in the liver, serves important protective functions. We investigated the effect of lowered tissue GSH content, accomplished by diethylmaleate (DEM) administration, on liver extracellular GSH levels before and after global ischemia in anesthetized rats. Liver extracellular GSH levels were determined by microdialysis perfusion and an on-line high performance liquid chromatography system. Global liver ischemia was induced by ligation of the hepatic pedicles including the hepatic artery, portal vein, and bile duct. DEM (4 mmol/kg) significantly lowered both the liver tissue GSH levels (1.36 +/- 0.26 micromol/g wet wt vs 9.50 +/- 0.55 micromol/g wet wt for the untreated) and the liver extracellular GSH levels (4.3 +/- 2.4 microM vs 25.2 +/- 8.7 microM for the untreated). Global liver ischemia induced a dramatic increase in the liver extracellular GSH level. Although the liver tissue GSH level was lowered following DEM treatment, DEM administration did not affect significantly ischemia-induced elevation of extracellular GSH (when presented as fold increase relative to basal value). In conclusion, DEM showed a direct effect on liver extracellular GSH content in anesthetized rats. However, DEM treatment did not affect the relative release of GSH following global liver ischemia.
谷胱甘肽（GSH）在肝脏中含量很高，具有重要的保护功能。我们研究了通过给予马来酸二乙酯（DEM）降低组织GSH含量对麻醉大鼠全脑缺血前后肝脏细胞外GSH水平的影响。肝脏细胞外GSH水平通过微透析灌注和在线高效液相色谱系统测定。通过结扎包括肝动脉、门静脉和胆管在内的肝蒂诱导全肝缺血。DEM（4 mmol/kg）显著降低了肝脏组织GSH水平（未处理组为9.50±0.55 μmol/g湿重，处理组为1.36±0.26 μmol/g湿重）和肝脏细胞外GSH水平（未处理组为25.2±8.7 μM，处理组为4.3±2.4 μM）。全肝缺血导致肝脏细胞外GSH水平急剧升高。尽管DEM处理后肝脏组织GSH水平降低，但DEM给药对缺血诱导的细胞外GSH升高没有显著影响（以相对于基础值的增加倍数表示）。总之，DEM对麻醉大鼠肝脏细胞外GSH含量有直接影响。然而，DEM处理不影响全肝缺血后GSH的相对释放。
