The Toxic Effects and Mechanism of Acetamiprid Exposure on Testicular Tissue: ALKBH5 Regulates m⁶A Modification to Affect PI3K-AKT-Mediated Apoptosis.
- 1Key Laboratory of Fertility Preservation and Maintenance of Ministry of Education, Ningxia Medical University, Yinchuan 750004, China.
- 2Key Laboratory of Environmental Factors and Chronic Disease Control, College of Public Health, Ningxia Medical University, Yinchuan 750004, China.
- 3Department of Toxicology, Shaanxi Provincial Key Lab of Free Radical Biology and Medicine, School of Public Health, Fourth Military Medical University, Xi'an 710032, China.
Abstract
(1) Background: Acetamiprid, a widely used neonicotinoid insecticide, has increasingly drawn people's attention to its potential reproductive toxicity risks. Although existing studies have shown that exposure to acetamiprid can cause testicular damage, its underlying molecular mechanism has not been fully elucidated. (2) Methods: This study established a mouse model of acetamiprid exposure via free drinking water and combined it with in vitro culture of TM3 cells, aiming to explore the toxic effects of acetamiprid on testicular tissue and its potential mechanism. (3) Results: Acetamiprid exposure induced significant pathological damage to the testicular tissue of mice and significantly reduced sperm quality. Further mechanism studies have shown that acetamiprid down-regulates the expression of RNA demethylase ALKBH5, leading to an overall increase in m⁶A modification levels, thereby inhibiting the activity of the PI3K/AKT signaling pathway and ultimately inducing apoptosis of TM3 cells. (4) Conclusions: In conclusion, this study, by integrating both internal and external models, has revealed a molecular mechanism by which acetamiprid is involved in testicular injury through epigenetic pathways, providing scientific basis and mechanism clues for assessing reproductive hazards caused by exposure to environmental toxins.
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BibTeX
@article{hua2026toxic,
title = {{The Toxic Effects and Mechanism of Acetamiprid Exposure on Testicular Tissue: ALKBH5 Regulates m⁶A Modification to Affect PI3K-AKT-Mediated Apoptosis.}},
author = {Xiaoyan Hua and Yubin Li and Lixiang Pang and Huiyuan Zhang and Yuwen Wang and Bing Wu and Haoxuan Gao and Yanan Song and Yucheng Yan and Huifang Yang and Yikai Qiu and Ji Zhao},
journal = {Toxics},
year = {2026},
month = oct,
doi = {10.3390/toxics14100903},
url = {https://europepmc.org/article/MED/42931690},
note = {CC BY},
}
RIS
TY - JOUR
TI - The Toxic Effects and Mechanism of Acetamiprid Exposure on Testicular Tissue: ALKBH5 Regulates m⁶A Modification to Affect PI3K-AKT-Mediated Apoptosis.
AU - Xiaoyan Hua
AU - Yubin Li
AU - Lixiang Pang
AU - Huiyuan Zhang
AU - Yuwen Wang
AU - Bing Wu
AU - Haoxuan Gao
AU - Yanan Song
AU - Yucheng Yan
AU - Huifang Yang
AU - Yikai Qiu
AU - Ji Zhao
PY - 2026
DA - 2026/10/12
JO - Toxics
DO - 10.3390/toxics14100903
UR - https://europepmc.org/article/MED/42931690
AB - (1) Background: Acetamiprid, a widely used neonicotinoid insecticide, has increasingly drawn people's attention to its potential reproductive toxicity risks. Although existing studies have shown that exposure to acetamiprid can cause testicular damage, its underlying molecular mechanism has not been fully elucidated. (2) Methods: This study established a mouse model of acetamiprid exposure via free drinking water and combined it with in vitro culture of TM3 cells, aiming to explore the toxic effects of acetamiprid on testicular tissue and its potential mechanism. (3) Results: Acetamiprid exposure induced significant pathological damage to the testicular tissue of mice and significantly reduced sperm quality. Further mechanism studies have shown that acetamiprid down-regulates the expression of RNA demethylase ALKBH5, leading to an overall increase in m⁶A modification levels, thereby inhibiting the activity of the PI3K/AKT signaling pathway and ultimately inducing apoptosis of TM3 cells. (4) Conclusions: In conclusion, this study, by integrating both internal and external models, has revealed a molecular mechanism by which acetamiprid is involved in testicular injury through epigenetic pathways, providing scientific basis and mechanism clues for assessing reproductive hazards caused by exposure to environmental toxins.
SN - 2305-6304
ER -