Raffin T A, Simon L M, Braun D, Theodore J, Robin E D
Lab Invest. 1980 Jun;42(6):622-6.
Exposure of isolated mouse lung macrophages to 40 and 60 per cent oxygen in tissue culture for 48 hours resulted in significant depression of phagocytosis as compared to air-exposed controls. The impairment of phagocytosis was reversed when the cells were reexposed to normoxic conditions for 48 hours. The impairment of phagocytosis occurred despite significant increases in intracellular superoxide dismutase activity, an enzyme felt to play a protective role in oxygen toxicity. Exposure to 40 and 60 per cent oxygen increased the susceptibility of lung macrophages to functional impairment by 95 per cent oxygen, rather than producing tolerance. The precise biologic and clinical significance of these findings will require additional studies in integrated systems. However, these studies show unequivocal lung macrophage injury with moderate hyperoxic exposure.
在组织培养中,将分离出的小鼠肺巨噬细胞暴露于40%和60%的氧气环境中48小时,与暴露于空气中的对照组相比,其吞噬作用显著降低。当细胞重新暴露于常氧环境48小时后,吞噬作用的损伤得以逆转。尽管细胞内超氧化物歧化酶活性显著增加(该酶被认为在氧中毒中起保护作用),但吞噬作用仍受到损害。暴露于40%和60%的氧气环境会使肺巨噬细胞对95%氧气导致的功能损害的易感性增加,而非产生耐受性。这些发现的确切生物学和临床意义需要在综合系统中进行更多研究。然而,这些研究表明,中度高氧暴露会明确导致肺巨噬细胞损伤。