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Tebuconazole Induces Mouse Fetal Testes Damage via ROS Generation in an Organ Culture Method
Won-Young Lee1, Ran Lee2, Hyun-Jung Park2
1Department of Livestock, Korea National University of Agriculture and Fisheries, Jeonju-si 54874, Republic of Korea.
Abstract:
The fungicide tebuconazole (TEB) poses risks to human and animal health via various exposure routes. It induces toxicity in multiple organs and disrupts reproductive health by affecting steroid hormone synthesis and fetal development. In this study, we investigated the impact of TEB on fetal testes using in vitro models, focusing on germ, Sertoli, and Leydig cells, and explored the mechanisms underlying cellular damage. The results revealed significant damage to germ cells and disruption of Leydig cell development. TEB exposure led to a decrease in germ cell numbers, as indicated by histological and immunostaining analyses. TEB induced the up- and down-regulation of the expression of fetal and adult Leydig cell markers, respectively. Additionally, TEB-treated fetal testes exhibited increased expression of oxidative-stress-related genes and proteins. However, co-treatment with the antioxidant N-acetylcysteine mitigated TEB-induced germ cell damage and prevented abnormal Leydig cell development. These findings suggest that administration of antioxidants can prevent the intratesticular damage typically caused by TEB exposure.
Insights
The fungicide tebuconazole (TEB) damages fetal testes by harming germ cells and disrupting Leydig cell development. Antioxidant treatment, such as N-acetylcysteine, can prevent this TEB-induced testicular toxicity.
Area of Science:
- Reproductive toxicology
- Environmental health
- Cellular biology
Background:
- Tebuconazole (TEB) is a widely used fungicide with known risks to human and animal health.
- TEB exposure can lead to organ toxicity and reproductive health issues, including effects on steroidogenesis and fetal development.
- Understanding TEB's impact on developing testes is crucial for assessing reproductive risks.
Purpose of the Study:
- To investigate the effects of TEB on fetal testes in vitro.
- To examine the mechanisms of TEB-induced cellular damage in fetal testicular cells (germ, Sertoli, and Leydig cells).
- To evaluate the protective potential of antioxidants against TEB toxicity in fetal testes.
Main Methods:
- Utilized in vitro models of fetal testes.
- Performed histological and immunostaining analyses to assess germ cell numbers and Leydig cell development.
- Analyzed the expression of fetal and adult Leydig cell markers.
- Quantified the expression of oxidative-stress-related genes and proteins.
- Investigated the effects of N-acetylcysteine (antioxidant) co-treatment.
Main Results:
- TEB exposure significantly reduced germ cell numbers in fetal testes.
- TEB disrupted Leydig cell development, altering the expression of their specific markers.
- TEB treatment increased the expression of oxidative-stress-related genes and proteins.
- N-acetylcysteine co-treatment effectively mitigated TEB-induced germ cell damage and prevented abnormal Leydig cell development.
Conclusions:
- TEB causes significant damage to fetal testicular cells, including germ and Leydig cells, partly through oxidative stress.
- Antioxidant administration, exemplified by N-acetylcysteine, can protect against TEB-induced testicular toxicity.
- These findings highlight the potential of antioxidants as a countermeasure for TEB-related reproductive harm.
