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Published on: October 4, 2019
Mentha piperita essential oil induces apoptosis in yeast associated with both cytosolic and mitochondrial
Patrícia Ferreira1, Teresa Cardoso, Filipa Ferreira
1Centre of Molecular and Environmental Biology (CBMA), Department of Biology, University of Minho, Braga, Portugal.
Abstract:
Mentha piperita (MP), also known as peppermint, is an aromatic and medicinal plant widely used in the food industry, perfumery and cosmetic, pharmacy and traditional medicine. Its essential oil (EO) displays antimicrobial activity against a range of bacteria and fungi. In this study, we found that MP EO lethal cytotoxicity is associated with increased levels of intracellular reactive oxygen species, mitochondrial fragmentation and chromatin condensation, without loss of the plasma membrane integrity, indicative of an apoptotic process. Overexpression of cytosolic catalase and superoxide dismutases reverted the lethal effects of the EO and of its major component menthol. Conversely, deficiency in Sod1p (cytosolic copper-zinc-superoxide dismutase) greatly increased sensitivity to both agents, but deficiency in Sod2p (mitochondrial manganese superoxide dismutase) only induced sensitivity under respiratory growth conditions. Mentha piperita EO increased the frequency of respiratory deficient mutants indicative of damage to the mitochondrial genome, although increase in mitochondrial thiol oxidation does not seem to be involved in the EO toxicity.
Insights
Mentha piperita essential oil induces cell death via apoptosis, involving reactive oxygen species and mitochondrial damage. Antioxidant enzymes like catalase and superoxide dismutases protect against its toxic effects.
Area of Science:
- Phytochemistry
- Cell Biology
- Toxicology
Background:
- Mentha piperita (peppermint) essential oil (EO) has diverse applications and known antimicrobial properties.
- Understanding the cellular mechanisms of MP EO toxicity is crucial for its safe application.
Purpose of the Study:
- To elucidate the cytotoxic mechanisms of Mentha piperita essential oil and its component menthol.
- To investigate the role of reactive oxygen species and antioxidant enzymes in MP EO-induced cell death.
Main Methods:
- Assessing cytotoxicity through reactive oxygen species levels, mitochondrial integrity, and chromatin condensation.
- Evaluating the effects of antioxidant enzyme overexpression and deficiencies (Sod1p, Sod2p) on cell survival.
- Analyzing the frequency of respiratory deficient mutants to detect mitochondrial genome damage.
Main Results:
- MP EO induces apoptosis via increased reactive oxygen species, mitochondrial fragmentation, and chromatin condensation without plasma membrane damage.
- Overexpression of catalase and superoxide dismutases mitigates EO and menthol toxicity.
- Sod1p deficiency enhances sensitivity, while Sod2p deficiency sensitivity is condition-dependent.
- MP EO increases respiratory deficient mutants, suggesting mitochondrial genome damage.
Conclusions:
- Mentha piperita essential oil triggers apoptosis through oxidative stress and mitochondrial pathways.
- Antioxidant enzymes play a significant role in cellular defense against MP EO toxicity.
- The mitochondrial genome is a potential target of MP EO, contributing to its cytotoxic effects.
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