Collinson L P, Dawes I W
School of Biochemistry and Molecular Genetics, University of New South Wales, Kensington, Australia.
J Gen Microbiol. 1992 Feb;138(2):329-335. doi: 10.1099/00221287-138-2-329.
Exponential phase cells of the yeast, Saccharomyces cerevisiae when treated with a non-lethal concentration of hydrogen peroxide (H2O2; 0.2mM) for 60 min adapted to become resistant to the lethal effects of a higher dose of H2O2 (2mM). From studies using cycloheximide to inhibit protein synthesis it appears that protein synthesis is required for maximal induction of resistance but that some degree of protection from the lethal effects of peroxide can be acquired in the absence of protein synthesis. Treatment of cells with 50 micrograms cycloheximide ml-1 alone lead to them acquiring some protection from peroxide. Cells subjected to heat shock became more resistant to 2mM-H2O2; however, peroxide pretreatment did not confer thermotolerance. L-[35S]Methionine labelling of cells subjected to 0.2 mM-H2O2 stress showed that synthesis of at least ten polypeptides was induced by peroxide treatment. Some of these were also induced in cells subjected to heat shock (23 to 37 degrees C shift) but the synthesis of at least four polypeptides (45, 39.5, 38 and 24 kDa) was unique to peroxide-stressed cells. Resistance to peroxide was also inducible in an isogenic petite and an isogenic strain with a mutation in the HAP1 gene, indicating that the adaptive response does not require functional mitochondria.
用非致死浓度的过氧化氢(H2O2;0.2mM)处理酿酒酵母指数期细胞60分钟后,这些细胞适应并变得对更高剂量的H2O2(2mM)的致死效应具有抗性。从使用环己酰亚胺抑制蛋白质合成的研究来看,似乎蛋白质合成对于抗性的最大诱导是必需的,但在没有蛋白质合成的情况下,也可以获得一定程度的免受过氧化物致死效应的保护。用50微克/毫升环己酰亚胺单独处理细胞会使它们获得一定程度的免受过氧化物的保护。经受热休克的细胞对2mM-H2O2更具抗性;然而,过氧化物预处理并未赋予耐热性。对经受0.2mM-H2O2胁迫的细胞进行L-[35S]甲硫氨酸标记显示,过氧化物处理诱导了至少十种多肽的合成。其中一些多肽在经受热休克(从23℃至37℃转变)的细胞中也被诱导,但至少四种多肽(45、39.5、38和24 kDa)的合成是过氧化物胁迫细胞所特有的。在同基因小菌落和HAP1基因突变的同基因菌株中,对过氧化物的抗性也可被诱导,这表明适应性反应不需要功能性线粒体。