期刊
BIOCHEMISTRY-MOSCOW
卷 79, 期 1, 页码 16-24出版社
MAIK NAUKA/INTERPERIODICA/SPRINGER
DOI: 10.1134/S0006297914010039
关键词
cycloheximide; Saccharomyces cerevisiae; thermotolerance; Hsp104; reactive oxygen species; programmed cell death
资金
- Ministry of Education and Science of Russian Federation [8266]
The mechanism of yeast cell death induced by heat shock was found to be dependent on the intensity of heat exposure. Moderate (45A degrees C) heat shock strongly increased the generation of reactive oxygen species (ROS) and cell death. Pretreatment with cycloheximide (at 30A degrees C) suppressed cell death, but produced no effect on ROS production. The protective effect was absent if cycloheximide was added immediately before heat exposure and the cells were incubated with the drug during the heat treatment and recovery period. The rate of ROS production and protective effect of cycloheximide on viability were significantly decreased in the case of severe (50A degrees C) heat shock. Treatment with cycloheximide at 39A degrees C inhibited the induction of Hsp104 synthesis and suppressed the development of induced thermotolerance to severe shock (50A degrees C), but it had no effect on induced thermotolerance to moderate (45A degrees C) heat shock. At the same time, Hsp104 effectively protected cells from death independently of the intensity of heat exposure. These data indicate that moderate heat shock induced programmed cell death in the yeast cells, and cycloheximide suppressed this process by inhibiting general synthesis of proteins.
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