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Hesperetin Induces Ferroptosis-Like Response in Saccharomyces cerevisiae
Huiwon Jang1, Dong Gun Lee1,2
1School of Life Sciences, BK21 FOUR KNU Creative BioResearch Group, Kyungpook National University, Daegu 41566, Republic of Korea.
Abstract:
Hesperetin has been reported to exhibit multiple beneficial activities, including anti-inflammatory and antimicrobial effects. It has also been shown to induce intracellular reactive oxygen species (ROS). However, its mode of action in fungi remains unclear. Therefore, this study aimed to clarify the underlying mechanisms of hesperetin using Saccharomyces cerevisiae as a model organism. Many antimicrobial compounds exert their effects by inducing oxidative damage in microbial cells. In this study, hesperetin increased intracellular reactive oxygen species in S. cerevisiae. This ROS accumulation was accompanied by glutathione depletion, indicating impaired antioxidant capacity and disrupted redox balance. Increased oxidative stress was also associated with an expanded pool of reactive iron, which can drive iron-dependent chemistry to generate highly reactive hydroxyl radicals. These radicals can initiate lipid peroxidation, leading to the accumulation of lipid hydroperoxides. Notably, these oxidative and lipid damage phenotypes were suppressed by ferrostatin-1, a ferroptosis inhibitor. In addition, apoptosis-associated hallmarks, including caspase activation and DNA fragmentation, were not observed under the same conditions. These findings indicate that hesperetin induces ferroptosis-like responses in S. cerevisiae, providing mechanistic insight into its antifungal effects.
Insights
Hesperetin induces fungal cell death by increasing reactive oxygen species (ROS) and iron, leading to ferroptosis-like responses. This mechanism clarifies its antimicrobial action against yeast.
Area of Science:
- Biochemistry
- Microbiology
- Cell Biology
Background:
- Hesperetin possesses known anti-inflammatory and antimicrobial properties.
- Its specific mechanism of action in fungi, particularly regarding oxidative stress, is not well understood.
Purpose of the Study:
- To elucidate the molecular mechanisms underlying hesperetin's antifungal activity.
- To investigate hesperetin's impact on oxidative stress and cell death pathways in *Saccharomyces cerevisiae*.
Main Methods:
- Hesperetin treatment of *Saccharomyces cerevisiae*.
- Measurement of intracellular reactive oxygen species (ROS) and glutathione levels.
- Assessment of reactive iron pools and lipid peroxidation.
- Evaluation of ferroptosis inhibition using ferrostatin-1.
- Analysis of apoptosis markers (caspase activation, DNA fragmentation).
Main Results:
- Hesperetin significantly increased intracellular ROS and depleted glutathione in *S. cerevisiae*, indicating impaired antioxidant capacity.
- Elevated reactive iron levels and subsequent lipid peroxidation were observed.
- Ferrostatin-1, a ferroptosis inhibitor, suppressed hesperetin-induced oxidative and lipid damage.
- No hallmarks of apoptosis were detected under hesperetin treatment.
Conclusions:
- Hesperetin induces a ferroptosis-like cell death pathway in *Saccharomyces cerevisiae*.
- The findings provide mechanistic insight into hesperetin's antifungal effects, highlighting its role in oxidative and lipid damage.
- This study clarifies hesperetin's mode of action by identifying ferroptosis as a key component.
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