Deneke S M, Bernstein S, Fanburg B L
Am Rev Respir Dis. 1978 Jul;118(1):105-11. doi: 10.1164/arrd.1978.118.1.105.
Mammalian cells may be protected from damage by hyperoxia through the induction of enzymes that reduce destructive oxygen-free radicals. One such enzyme is superoxide dismutase, which reduces superoxide to form hydrogen peroxide and O2. We studied the concentration of this enzyme in rat alveolar macrophages exposed to 85 to 90 per cent O2 in vitro for as long as 6 days and in macrophages obtained from rats exposed to 85 to 97 per cent O2 in vivo for as long as 7 days. In no case was there an increase in superoxide dismutase in rat alveolar macrophages, despite a doubling of superoxide dismutase in whole lungs of rats exposed to 85 to 90 per cent O2 for 7 days in vivo. We concluded that the macrophage of the adult rat does not defent itself against hyperoxia by the induction of superoxide dismutase and does not participate in the increased superoxide dismutase activity of lungs of these animals exposed to hyperoxia.
哺乳动物细胞可通过诱导产生能减少破坏性氧自由基的酶来免受高氧损伤。其中一种酶是超氧化物歧化酶,它能将超氧化物还原为过氧化氢和氧气。我们研究了体外暴露于85%至90%氧气长达6天的大鼠肺泡巨噬细胞以及体内暴露于85%至97%氧气长达7天的大鼠所获得的巨噬细胞中这种酶的浓度。在任何情况下,大鼠肺泡巨噬细胞中的超氧化物歧化酶都没有增加,尽管在体内暴露于85%至90%氧气7天的大鼠全肺中超氧化物歧化酶增加了一倍。我们得出结论,成年大鼠的巨噬细胞不会通过诱导超氧化物歧化酶来抵御高氧,也不参与这些暴露于高氧环境的动物肺部超氧化物歧化酶活性的增加。