Kaneko M, Kodama M, Inoue F, Terasaki T
National Cancer Center Research Institute, Tokyo, Japan.
Free Radic Res. 1996 Apr;24(4):299-309. doi: 10.3109/10715769609088027.
The mechanism of H2O2-resistance of Hpr-4, a variant of Chinese hamster V79 cells, was investigated. The effect of H2O2 on the mitochondria of the parental and Hpr-4 cells was compared. First, both biochemical and ultrastructural results showed that mitochondria in the parental cells were damaged by exposure to H2O2, while those in Hpr-4 cells recovered from the damage. Second, the H2O2-resistance of Hpr-4 cells was reversibly reduced or recovered by the addition or removal of inhibitors of mitochondrial biosynthesis, respectively. Third, the parental cells were auxotrophic to pyruvate after exposure to H2O2. Fourth, H2O2-sensitivity of the parental cells was also enhanced by the inhibition of mitochondrial biosynthesis. From these results, it was concluded that the mitochondria of Hpr-4 cells apparently had a greater resistance to H2O2 than those of the parental cells and that functional mitochondria were involved in the recovery of Chinese hamster V79 cells from H2O2-induced damage.
对中国仓鼠V79细胞变体Hpr-4的过氧化氢抗性机制进行了研究。比较了过氧化氢对亲代细胞和Hpr-4细胞线粒体的影响。首先,生化和超微结构结果均表明,亲代细胞中的线粒体因暴露于过氧化氢而受损,而Hpr-4细胞中的线粒体则从损伤中恢复。其次,分别添加或去除线粒体生物合成抑制剂可使Hpr-4细胞的过氧化氢抗性可逆地降低或恢复。第三,亲代细胞在暴露于过氧化氢后对丙酮酸营养缺陷。第四,抑制线粒体生物合成也增强了亲代细胞对过氧化氢的敏感性。从这些结果可以得出结论,Hpr-4细胞的线粒体对过氧化氢的抗性明显高于亲代细胞,并且功能性线粒体参与了中国仓鼠V79细胞从过氧化氢诱导的损伤中恢复的过程。