Jenkinson S G, Long R J, Lawrence R A
J Lab Clin Med. 1984 Jan;103(1):143-51.
Rats treated with low doses of bacterial endotoxin have been shown to be protected from oxygen poisoning under normobaric conditions. Induction of lung activity of the antioxidant enzymes glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), and catalase (CAT) has been reported to occur with endotoxin administration. GSH-Px is a selenoenzyme and selenium-deficient rats have decreased lung GSH-Px activity and enhanced lung toxicity during a hyperoxic exposure. To determine whether bacterial endotoxin administration can provide protection for animals with decreased antioxidant defenses, selenium-deficient and control rats received daily intraperitoneal injections of 250 micrograms/kg bacterial endotoxin or phosphate-buffered saline (PBS) during normobaric exposure to greater than 95% O2. Both groups of animals were protected from hyperoxia by bacterial endotoxin administration despite the extremely low lung GSH-Px activity in the selenium-deficient rats. GSH-Px, SOD, or CAT activities were not induced in the selenium-deficient rats by 48 hr (the time when the selenium-deficient rats treated with PBS began to die). In the selenium-deficient rat, mechanisms other than enzyme induction appear to be providing early protection from hyperoxia.
已表明，用低剂量细菌内毒素处理的大鼠在常压条件下可免受氧中毒。据报道，给予内毒素后，抗氧化酶谷胱甘肽过氧化物酶（GSH-Px）、超氧化物歧化酶（SOD）和过氧化氢酶（CAT）的肺活性会被诱导。GSH-Px是一种含硒酶，缺硒大鼠在高氧暴露期间肺GSH-Px活性降低且肺毒性增强。为了确定给予细菌内毒素是否能为抗氧化防御能力下降的动物提供保护，缺硒大鼠和对照大鼠在常压下暴露于大于95% O₂期间，每天腹腔注射250微克/千克细菌内毒素或磷酸盐缓冲盐水（PBS）。尽管缺硒大鼠的肺GSH-Px活性极低，但两组动物通过给予细菌内毒素均免受高氧影响。缺硒大鼠在48小时内（即用PBS处理的缺硒大鼠开始死亡的时间）未诱导出GSH-Px、SOD或CAT活性。在缺硒大鼠中，除酶诱导外的其他机制似乎在为其提供免受高氧影响的早期保护。
