ROS production by adrenodoxin does not cause apoptosis in fission yeast

被引:15
作者
Derouet-Huembert, Evi
Dragan, Calin-Aurel
Hakki, Tarek
Bureik, Matthias
机构
[1] Univ Saarland, Dept Biochem, D-66041 Saarbrucken, Germany
[2] Univ Saarland, Starterzentrum, PomBioTech GmbH, D-66123 Saarbrucken, Germany
关键词
adrenodoxin; apoptosis; cytochrome P450 system; fission yeast; mitochondria; reactive oxygen species;
D O I
10.1007/s10495-007-0133-1
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
We previously showed that production of reactive oxygen species (ROS) caused by overexpression of the mitochondrial electron transfer protein adrenodoxin (Adx) induces apoptosis in mammalian cells. In the fission yeast Schizosaccharomyces pombe, ROS are also produced in cells that undergo an apoptotic-like cell death, but it is not yet clear whether they are actually causative for this phenomenon or whether they are merely produced as a by-product. Therefore, the purpose of this study was to trigger mitochondrial ROS production in fission yeast by overexpression of either wildtype Adx (Adx-WT) or of several activated Adx mutants and to investigate its consequences. It was found that strong expression of either Adx-WT or Adx- S112W did not produce any ROS, while Adx- D113Y caused a twofold and Adx(1-108) a threefold increase in ROS formation as compared to basal levels. However, no typical apoptotic markers or decreased viability could be observed in these strains. Since we previously observed that an increase in mitochondrial ROS formation of about 60% above basal levels is sufficient to strongly induce apoptosis in mammalian cells, we conclude that S. pombe is either very robust to mitochondrial ROS production or does not undergo apoptotic cell death in response to mitochondrial ROS at all.
引用
收藏
页码:2135 / 2142
页数:8
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