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Published on: April 11, 2021
Effect of aspirin on mitochondrial mutagens in Saccharomyces cerevisiae
Abstract:
The mitochondrial mutation petite was induced in yeast cells by ethidium bromide (EB), Adriamycin (ADR) and 4-nitroquinoline-N-oxide (NQO). In the presence of aspirin in concentrations ranging from 0.1 to 1.0 mg/ml, the mutagenicity of EB and ADR was reversed but petite induction by NQO was unaffected. At these concentrations, aspirin also reversed mitochondrial inhibition by oligomycin, a non-mutagenic inhibitor of the organellar ATPase complex. Cells grown in the presence of aspirin alone showed a significantly higher rate of oxygen uptake than untreated control cultures when the drug concentration ranged from 0.05 to 1.0 mg/ml. At concentrations of 2 mg/ml and above, aspirin inhibited mitochondrial respiration.
Insights
Aspirin reversed mitochondrial mutations induced by ethidium bromide and Adriamycin in yeast. However, it did not affect NQO-induced mutations but enhanced oxygen consumption at low doses.
Area of Science:
- Mitochondrial genetics
- Yeast cell biology
- Drug toxicology
Background:
- Mitochondrial mutations, such as the petite phenotype in yeast, can be induced by various chemical mutagens.
- Ethidium bromide (EB), Adriamycin (ADR), and 4-nitroquinoline-N-oxide (NQO) are known inducers of mitochondrial petite mutations.
- Aspirin's effects on mitochondrial function and mutagenicity are not fully understood.
Purpose of the Study:
- To investigate the effect of aspirin on the mutagenicity of EB, ADR, and NQO in yeast.
- To determine aspirin's impact on mitochondrial inhibition caused by oligomycin.
- To assess aspirin's influence on cellular respiration and oxygen uptake.
Main Methods:
- Induction of petite mutations in yeast using EB, ADR, and NQO.
- Treatment of yeast cells with varying concentrations of aspirin in the presence of mutagens.
- Measurement of mitochondrial inhibition reversal by aspirin using oligomycin.
- Assay of oxygen uptake rates in yeast cells treated with aspirin.
Main Results:
- Aspirin (0.1–1.0 mg/ml) reversed the mutagenicity of EB and ADR but not NQO.
- Aspirin at the same concentrations reversed mitochondrial inhibition by oligomycin.
- Low aspirin concentrations (0.05–1.0 mg/ml) significantly increased oxygen uptake.
- High aspirin concentrations (≥2 mg/ml) inhibited mitochondrial respiration.
Conclusions:
- Aspirin exhibits protective effects against specific mitochondrial mutagens (EB, ADR) in yeast.
- Aspirin can ameliorate oligomycin-induced mitochondrial inhibition.
- Aspirin modulates yeast mitochondrial respiration, enhancing it at low doses and inhibiting it at high doses.
