ArticleProceedings of the National Academy of Sciences of the United States of America1996
Oxidative stress is involved in heat-induced cell death in Saccharomyces cerevisiae.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 120 papers.
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Who cites it
120 citing papers in PubMed, 441 citations in OpenAlex.
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- The intricate role of Sir2 in oxidative stress response during the post-diauxic phase inFrontiers in microbiology · 2023Article
- MetA is a "thermal fuse" that inhibits growth and protects Escherichia coli at elevated temperatures.Cell reports · 2022Article
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- A novel gene from the acidophilic bacterium Leptospirillum sp. CF-1 and its role in oxidative stress and chromate tolerance.Biological research · 2022Article
- Distinct Metabolic Flow in Response to Temperature in Thermotolerant Kluyveromyces marxianus.Applied and environmental microbiology · 2022Article
- Kveik Brewing Yeasts Demonstrate Wide Flexibility in Beer Fermentation Temperature Tolerance and Exhibit Enhanced Trehalose Accumulation.Frontiers in microbiology · 2022Article
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- Physiological and Molecular Characterization of an Oxidative Stress-ResistantFrontiers in microbiology · 2022Article
60 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The cause for death after lethal heat shock is not well understood. A shift from low to intermediate temperature causes the induction of heat-shock proteins in most organisms. However, except for HSP104, a convincing involvement of heat-shock proteins in the development of stress resistance has not been established in Saccharomyces cerevisiae. This paper shows that oxidative stress and antioxidant enzymes play a major role in heat-induced cell death in yeast. Mutants deleted for the antioxidant genes catalase, superoxide dismutase, and cytochrome c peroxidase were more sensitive to the lethal effect of heat than isogenic wild-type cells. Overexpression of catalase and superoxide dismutase genes caused an increase in thermotolerance. Anaerobic conditions caused a 500- to 20,000-fold increase in thermotolerance. The thermotolerance of cells in anaerobic conditions was immediately abolished upon oxygen exposure. HSP104 is not responsible for the increased resistance of anaerobically grown cells. The thermotolerance of anaerobically grown cells is not due to expression of heat-shock proteins. By using an oxidation-dependent fluorescent molecular probe a 2- to 3-fold increase in fluorescence was found upon heating. Thus, we conclude that oxidative stress is involved in heat-induced cell death.
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