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Updated: Aug 16, 2026
Flow Cytometric Analysis of Mitochondrial Reactive Oxygen Species in Murine Hematopoietic Stem and Progenitor Cells and MLL-AF9 Driven Leukemia
Published on: September 5, 2019
Maltol/iron-mediated apoptosis in HL60 cells: participation of reactive oxygen species
Keiko Murakami1, Kumiko Ishida, Kyoko Watakabe
1Department of Biochemistry, Aichi Medical University School of Medicine, Yazako, Nagakute, Aichi 480-1195, Japan.
Abstract:
Apoptosis of HL60 cells by maltol was analyzed in relation to the maltol/iron-mediated generation of reactive oxygen species. Addition of maltol with FeSO(4) induced an apoptotic cell death as judged by flow cytometry analysis and DNA fragmentation on electrophoresis, but maltol or iron alone did not affect the cells. Treatment of HL60 cells with maltol/iron complex caused an effective inactivation of aconitase the most sensitive enzyme to reactive oxygen species. Maltol/iron-mediated apoptosis and the inactivation of aconitase was prevented by TEMPOL, the scavenger of reactive oxygen species. These findings suggest that maltol/iron complex can generate reactive oxygen species by the redox cycling, resulting in an apoptosis of HL60 cells. Cytotoxicity of maltol can be explained by the prooxidant properties of this compound.
Insights
Maltol combined with iron induces cancer cell death (apoptosis) by generating harmful reactive oxygen species. This prooxidant effect explains maltol's cytotoxicity.
Area of Science:
- Biochemistry
- Cell Biology
- Toxicology
Background:
- Maltol is a compound found in various foods.
- The cytotoxic mechanisms of maltol are not fully understood.
- Iron is essential for cellular processes but can also mediate oxidative stress.
Purpose of the Study:
- To investigate the role of reactive oxygen species (ROS) in maltol-induced apoptosis of HL60 cells.
- To elucidate the mechanism of maltol/iron complex-mediated cytotoxicity.
Main Methods:
- HL60 cells were treated with maltol and/or iron (FeSO4).
- Apoptosis was assessed using flow cytometry and DNA fragmentation analysis.
- Aconitase activity, a marker sensitive to ROS, was measured.
- The effect of TEMPOL, a ROS scavenger, was evaluated.
Main Results:
- Maltol/iron complex induced significant apoptotic cell death in HL60 cells.
- Neither maltol nor iron alone caused apoptosis.
- Maltol/iron treatment led to effective inactivation of aconitase.
- TEMPOL treatment prevented both maltol/iron-induced apoptosis and aconitase inactivation.
Conclusions:
- Maltol/iron complex generates ROS via redox cycling, leading to HL60 cell apoptosis.
- The prooxidant properties of maltol contribute to its cytotoxicity.
- Targeting ROS may be a strategy to mitigate maltol toxicity.
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