关键词: fetal testes germ cell reactive oxygen species tebuconazole

Mesh : Male Animals Testis / drug effects metabolism Triazoles / pharmacology Mice Reactive Oxygen Species / metabolism Leydig Cells / drug effects metabolism Oxidative Stress / drug effects Organ Culture Techniques / methods Sertoli Cells / drug effects metabolism Antioxidants / pharmacology Fetus / drug effects Fungicides, Industrial / toxicity Germ Cells / drug effects metabolism

来  源:   DOI:10.3390/ijms25137050   PDF(Pubmed)

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.
摘要:
杀菌剂戊唑醇(TEB)通过各种暴露途径对人类和动物健康构成风险。它在多个器官中诱导毒性,并通过影响类固醇激素合成和胎儿发育来破坏生殖健康。在这项研究中,我们使用体外模型研究了TEB对胎儿睾丸的影响,专注于细菌,Sertoli,和Leydig细胞,并探索了细胞损伤的潜在机制。结果表明,生殖细胞受到严重损害,睾丸间质细胞发育遭到破坏。TEB暴露导致生殖细胞数量减少,如组织学和免疫染色分析所示。TEB诱导胎儿和成年睾丸间质细胞标志物表达的上调和下调,分别。此外,TEB处理的胎儿睾丸显示氧化应激相关基因和蛋白质的表达增加。然而,与抗氧化剂N-乙酰半胱氨酸共同处理减轻了TEB诱导的生殖细胞损伤并防止了异常的Leydig细胞发育。这些发现表明,抗氧化剂的施用可以预防通常由TEB暴露引起的睾丸内损伤。
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