Mixtures of glyphosate and surfactant TN20 accelerate cell death via mitochondrial damage-induced apoptosis and necrosis
- Abstract
- Glyphosate, a common herbicide, is not toxic under normal exposure circumstances. However, this chemical, when combined with a surfactant, is cytotoxic. In this study, the mechanism of the additive effect of glyphosate and TN-20, a common surfactant in glyphosate herbicides, was investigated. After exposure of rat H9c2 cells to glyphosate and TN-20 mixtures, following assays were performed: flow cytometry to determine the proportion of cells that underwent apoptosis and necrosis; western blotting to determine expression of mitochondrial proteins (Bcl-2 and Bax); immunological methods to evaluate translocation of cytochrome C; luminometric measurements to determine activity of caspases 3/7 and 9; and tetramethyl rhodamine methyl ester assay to measure mitochondrial membrane potentials. Bcl-1 intensity decreased while Bax intensity increased with exposure to increasing TN-20 and/or glyphosate concentrations. Caspase activity increased and mitochondrial membrane potential decreased only when the cells were exposed to a mixture of both TN-20 and glyphosate, but not after exposure to either one of these compounds. The results support the possibility that mixtures of glyphosate and TN-20 aggravate mitochondrial damage and induce apoptosis and necrosis. Throughout this process, TN-20 seems to disrupt the integrity of the cellular barrier to glyphosate uptake, promoting glyphosate-mediated toxicity.
- All Author(s)
- Y. H. Kim
; J. R. Hong
; H. W. Gil
; H. Y. Song
; S. Y. Hong
- Issued Date
- 2013
- Type
- Article
- Keyword
- Glyphosate; Surfactant; Mitochondrial damage; Apoptosis; Necrosis
- Publisher
- British Industrial Biological Research Association
- ISSN
- 0887-2333
; 1879-3177
- Citation Title
- Toxicology in vitro
- Citation Volume
- 27
- Citation Number
- 1
- Citation Start Page
- 191
- Citation End Page
- 197
- Language(ISO)
- eng
- DOI
- 10.1016/j.tiv.2012.09.021
- URI
- http://schca-ir.schmc.ac.kr/handle/2022.oak/1913
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