Polyethylene glycol-attached antioxidant enzymes decrease pulmonary oxygen toxicity in rats.
Polyethylene glycol-attached antioxidant enzymes decrease pulmonary oxygen toxicity in rats.
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聚乙二醇附着的抗氧化酶可降低大鼠的肺氧毒性。
DOI：
10.1152/jappl.1989.66.2.584
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发表时间：
1989
期刊：
影响因子：
--
通讯作者：
Repine,JE
中科院分区：
文献类型：
--
作者：
White,CW;Jackson,JH;Abuchowski,A;Kazo,GM;Mimmack,RF;Berger,EM;Freeman,BA;McCord,JM;Repine,JE
当连续暴露于高氧（100%O2，760 Torr大气压）时，用聚乙二醇（PEG）连接的超氧化物歧化酶和过氧化氢酶（PEG-SOD + PEG-CAT）预处理的大鼠比用盐水（60.7 +/- 2.1 h）或PEG灭活的SOD + PEG灭活的CAT（62.3 +/- 1.6 h）预处理的大鼠寿命更长（79.1 ± 7.6 h）。PEG-SOD + PEG-CAT预处理的大鼠也有较少的高氧诱导的急性氧化性水肿性肺损伤，肺氧化型谷胱甘肽（GSSG）含量的增加，胸腔积液，肺灌洗液白蛋白浓度比盐水预处理的大鼠进行评估。与用PEG、SOD + CAT + PEG、SOD + CAT或生理盐水预处理的大鼠相比，用长寿命缀合物PEG-失活-SOD + PEG-失活-CAT或PEG-白蛋白预处理的大鼠也具有减少的急性氧化性水肿性肺损伤。体外研究表明，PEG本身可能通过清除羟基自由基（.OH）而不是超氧阴离子（O2-）来起到保护作用。或H2 O2。与用于增加肺抗氧化酶的更有效的内源性（通过预暴露于缺氧）或外源性（通过脂质体）手段相比，PEG酶对来自连续高氧的肺损伤的保护性较小。
When exposed continuously to hyperoxia (100% O2, 760 Torr barometric pressure), rats pretreated with polyethylene glycol (PEG)-attached superoxide dismutase and catalase (PEG-SOD + PEG-CAT) lived longer (79.1 + 7.6 h) than rats pretreated with saline (60.7 +/- 2.1 h) or PEG-inactivated-SOD + PEG-inactivated-CAT (62.3 +/- 1.6 h). Rats pretreated with PEG-SOD + PEG-CAT also had less hyperoxia-induced acute oxidative edematous lung injury, as assessed by increases in lung oxidized glutathione (GSSG) contents, pleural effusions, and lung lavage albumin concentrations than saline-pretreated rats. Rats pretreated with the long-lived conjugates PEG-inactivated-SOD + PEG-inactivated-CAT or PEG-albumin also had decreased acute oxidative edematous lung injury compared with rats pretreated with PEG, SOD + CAT + PEG, SOD + CAT, or saline. In vitro studies suggested that PEG itself may have contributed to protection by scavenging hydroxyl radical (.OH) but not superoxide (O2-.) or H2O2. Compared with more effective endogenous (via preexposure to hypoxia) or exogenous (via liposomes) means for increasing lung antioxidant enzymes, PEG enzymes are less protective against lung injury from continuous hyperoxia.