Othmène Yosra Ben, Salem Intidhar Ben, Hamdi Hiba, Annabi Emna, Abid-Essefi Salwa
University of Monastir, Faculty of Dental Medicine, Laboratory for Research on Biologically Compatible Compounds, LR01SE17, Avicenne Street, 5000 Monastir, Tunisia; Higher Institute of Biotechnology, University of Monastir, Taher Haddad Street, 5000, Monastie, Tunisia.
University of Monastir, Faculty of Dental Medicine, Laboratory for Research on Biologically Compatible Compounds, LR01SE17, Avicenne Street, 5000 Monastir, Tunisia; Higher Institute of Biotechnology, University of Monastir, Taher Haddad Street, 5000, Monastie, Tunisia; University of Sousse, Faculty of Medicine of Sousse, 4000, Tunisia.
Pestic Biochem Physiol. 2021 May;174:104797. doi: 10.1016/j.pestbp.2021.104797. Epub 2021 Feb 11.
Tebuconazole (TEB) is a common triazole fungicide that has been widely used for the control of plant pathogenic fungi, suggesting that mammal exposure occurs regularly. Several studies demonstrated that TEB exposure has been linked to a variety of toxic effects, including neurotoxicity, immunotoxicity, reprotoxicity and carcinogenicity. However, there is a few available data regarding the molecular mechanism involved in TEB-induced toxicity. The current study was undertaken to investigate the toxic effects of TEB in HCT116 cells. Our results showed that TEB caused cytotoxicity by inhibiting cell viability as assessed by the MTT assay. Furthermore, we have demonstrated that TEB induced a significant increase in the reactive oxygen species (ROS) production leading to the induction of lipid peroxidation and DNA fragmentation and increased superoxide dismutase (SOD) and catalase (CAT) activities. Moreover, TEB exposure induced mitochondrial membrane potential loss and caspase-9/-3 activation. Treatment with general caspases inhibitor (Z-VAD-fmk) significantly prevented the TEB-induced cell death, indicating that TEB induced caspases-dependent cell death. These findings suggest the involvement of oxidative stress and apoptosis in TEB-induced toxicity in HCT116.
戊唑醇（TEB）是一种常见的三唑类杀菌剂，已被广泛用于防治植物病原真菌，这表明哺乳动物经常接触到它。多项研究表明，接触戊唑醇与多种毒性作用有关，包括神经毒性、免疫毒性、生殖毒性和致癌性。然而，关于戊唑醇诱导毒性的分子机制，现有数据较少。本研究旨在探讨戊唑醇对HCT116细胞的毒性作用。我们的结果表明，通过MTT法评估，戊唑醇通过抑制细胞活力导致细胞毒性。此外，我们证明戊唑醇诱导活性氧（ROS）产生显著增加，导致脂质过氧化和DNA片段化，并增加超氧化物歧化酶（SOD）和过氧化氢酶（CAT）活性。此外，接触戊唑醇会导致线粒体膜电位丧失和半胱天冬酶-9/-3激活。用通用半胱天冬酶抑制剂（Z-VAD-fmk）处理可显著预防戊唑醇诱导的细胞死亡，表明戊唑醇诱导半胱天冬酶依赖性细胞死亡。这些发现表明氧化应激和细胞凋亡参与了戊唑醇对HCT116细胞的毒性作用。
