Almagor M, Kahane I, Yatziv S
J Clin Invest. 1984 Mar;73(3):842-7. doi: 10.1172/JCI111279.
The role of Mycoplasma pneumoniae-generated superoxide and hydrogen peroxide in inducing host cell injury was studied in normal and trisomy 21 human cells. As a result of M. pneumoniae infection, catalase activity in infected normal skin fibroblasts and ciliated epithelial cells decreased by 74-77% as compared with uninfected controls. Addition of superoxide dismutase to the infected cultured cells totally prevented the inhibition whereas addition of catalase or catalytically inactivated superoxide dismutase had no protective effect. Trisomy 21 erythrocytes and cultured skin fibroblasts in which CuZn-superoxide dismutase content is 50% greater than in normal cells were infected by M. pneumoniae. The inhibition of catalase activity in these cells was 7-33% and 0-20.5%, respectively, as compared with 65-72% and 48-68% inhibition in normal infected controls. Following M. pneumoniae infection, the levels of malonyldialdehyde, an indicator for membrane lipid peroxidation were raised in trisomy 21 cultured fibroblasts by 10-32% while in normal cells malonyldialdehyde increased by 140-870%. Externally added superoxide dismutase, but not catalase, reduced the extent of lipid peroxidation in normal infected cells. Lactate dehydrogenase release from normal infected cells was time correlated with the increase in their malonyldialdehyde formation. It is suggested that superoxide generated during M. pneumoniae infection is involved in the inhibition of host cell catalase activity. The inactivation of this cellular antioxidative defense mechanism results in progressive oxidative damage to the M. pneumoniae-infected cells.
在正常和21三体人类细胞中研究了肺炎支原体产生的超氧化物和过氧化氢在诱导宿主细胞损伤中的作用。肺炎支原体感染后，与未感染的对照相比，感染的正常皮肤成纤维细胞和纤毛上皮细胞中的过氧化氢酶活性降低了74 - 77%。向感染的培养细胞中添加超氧化物歧化酶完全阻止了这种抑制作用，而添加过氧化氢酶或催化失活的超氧化物歧化酶则没有保护作用。肺炎支原体感染了21三体红细胞和培养的皮肤成纤维细胞，其中铜锌超氧化物歧化酶含量比正常细胞高50%。与正常感染对照中65 - 72%和48 - 68%的抑制率相比，这些细胞中过氧化氢酶活性的抑制率分别为7 - 33%和0 - 20.5%。肺炎支原体感染后，21三体培养成纤维细胞中膜脂质过氧化指标丙二醛的水平升高了10 - 32%，而正常细胞中丙二醛增加了140 - 870%。外部添加的超氧化物歧化酶而非过氧化氢酶降低了正常感染细胞中的脂质过氧化程度。正常感染细胞中乳酸脱氢酶的释放与它们丙二醛形成的增加呈时间相关性。提示肺炎支原体感染期间产生的超氧化物参与了宿主细胞过氧化氢酶活性的抑制。这种细胞抗氧化防御机制的失活导致肺炎支原体感染细胞的渐进性氧化损伤。
