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Direct exposure to vinclozolin induces sex-dependent mitochondrial dysfunction in mouse liver
Hwayeon Lim1,2, Jisun Choi3, Joo Young Huh4,5
1Department of Biomedical Engineering, The Ohio State University, Columbus, OH 43210, USA.
Current Research in Toxicology
|June 15, 2026
Summary
Vinclozolin exposure impairs mitochondrial function and energy production. This endocrine disruptor affects citrate synthase and complex IV activity, with sex-specific antioxidant responses observed in mouse liver mitochondria.
Area of Science:
- Environmental Toxicology
- Mitochondrial Biology
- Endocrinology
Background:
- Vinclozolin is an anti-androgenic fungicide with endocrine-disrupting effects.
- Endocrine disruptors are linked to impaired mitochondrial function, reduced ATP production, and metabolic diseases.
- Direct toxicity of vinclozolin on mitochondrial function requires further investigation.
Purpose of the Study:
- To investigate the direct impact of vinclozolin exposure on mouse liver mitochondria.
- To assess vinclozolin's effects on key mitochondrial function markers and oxidative stress.
- To determine if vinclozolin's mitochondrial toxicity exhibits sex-specific differences.
Main Methods:
- Isolated mitochondria from mouse liver were directly exposed to vinclozolin.
- Measured citrate synthase activity, mitochondrial complex IV (CIV) activity, and ATP production.
- Assessed reactive oxygen/nitrogen species (ROS/RNS), cytochrome c release, glutathione (GSH) levels, and superoxide dismutase (SOD) activity.
Main Results:
- Vinclozolin decreased citrate synthase activity in both sexes and CIV activity in males.
- ATP production tended to decrease, while ROS/RNS levels tended to increase, particularly in males.
- SOD activity increased sex-dependently in females; cytochrome c release increased in both sexes.
Conclusions:
- Direct mitochondrial exposure to vinclozolin induces dysfunction and impairs energy production.
- Vinclozolin's effects on mitochondrial function are mediated by sex-specific antioxidant responses.
- These findings highlight vinclozolin's potential to disrupt cellular energy metabolism through direct mitochondrial toxicity.
