Räder L, Siems W, Müller M, Gerber G
Cell Biochem Funct. 1985 Oct;3(4):289-96. doi: 10.1002/cbf.290030408.
The biliary GSSG efflux rate of normoxic perfused rat liver was 1.5 +/- 0.2 nmol/min/g liver wet weight. The GSSG efflux rate as indicator for the flux through the glutathione peroxidase reaction and, therefore, for an oxidative loading increased with the extent of hypoxia. 2.6 +/- 0.5 nmol/min/g were released from the severely hypoxic liver. The hydroxyl radical scavenger formate as well as the xanthine oxidase inhibitor allopurinol reduced the efflux rate of GSSG. GSH was released from the perfused liver at a rate of 15.5 nmol/min/g which was nearly unchanged in severe hypoxia. The high rate of glucose liberation from the hypoxic liver declined to almost that of the normoxic organ in the presence of formate. There is an 'oxidative stress' during hypoxic liver perfusion which probably originates from increased generation of activated oxygen species in the degradation of purine nucleotides.
正常氧合灌注大鼠肝脏的胆汁谷胱甘肽二硫化物（GSSG）流出率为1.5±0.2纳摩尔/分钟/克肝脏湿重。GSSG流出率作为谷胱甘肽过氧化物酶反应通量的指标，因此也是氧化负荷的指标，随着缺氧程度的增加而升高。严重缺氧的肝脏释放出2.6±0.5纳摩尔/分钟/克。羟基自由基清除剂甲酸盐以及黄嘌呤氧化酶抑制剂别嘌呤醇降低了GSSG的流出率。谷胱甘肽（GSH）从灌注肝脏的释放速率为15.5纳摩尔/分钟/克，在严重缺氧时几乎没有变化。在甲酸盐存在的情况下，缺氧肝脏中高比率的葡萄糖释放下降至几乎与正常氧合器官相同的水平。缺氧肝脏灌注期间存在“氧化应激”，这可能源于嘌呤核苷酸降解过程中活性氧生成的增加。
