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Hexaconazole-Induced Male Reproductive Toxicity Through ROS-Mediated Ferroptosis and Impaired Leydig Cell
Ran Lee1,2, Hyeon Woo Sim3, Won-Young Lee1
1Department of Livestock, Korea National University of Agriculture and Fisheries, Jeonju-si 54874, Jeonbuk, Republic of Korea.
International Journal of Molecular Sciences
|July 28, 2026
Summary
Hexaconazole (HEX), a triazole fungicide, impairs male fertility by reducing sperm motility and testosterone. It induces ferroptosis, a cell death pathway, in Leydig cells, disrupting reproductive health.
Area of Science:
- Environmental Toxicology
- Reproductive Toxicology
- Cell Death Mechanisms
Background:
- Triazole fungicides are widespread environmental pollutants.
- Their impact on male reproductive health is not fully understood.
Purpose of the Study:
- To investigate the toxicological effects of hexaconazole (HEX) on testicular function in mice.
- To elucidate the molecular mechanisms underlying HEX-induced reproductive toxicity.
Main Methods:
- Mice were administered HEX for 8 weeks.
- Sperm motility, testosterone levels, gene expression (germ cell, meiotic, steroidogenic markers), reactive oxygen species (ROS), and ferroptosis markers were assessed.
- In vitro studies used primary Leydig cells.
Main Results:
- HEX significantly reduced sperm motility and testosterone levels.
- HEX downregulated germ cell and meiotic markers, and steroidogenic genes.
- HEX induced ROS production and ferroptosis in Leydig cells, characterized by iron accumulation, lipid peroxidation, and altered ferroptosis regulators (e.g., Gpx4 depletion).
- In vitro, HEX compromised Leydig cell viability and steroidogenesis.
Conclusions:
- Leydig cell ferroptosis is a key mechanism in HEX-induced male reproductive toxicity.
- This links endocrine disruption to impaired spermatogenesis.
- Targeting the ferroptosis-mediated antioxidant defense system may mitigate risks from triazole fungicide exposure.
