Ma, Xinyan et al. published their research in International Journal of Molecular Medicine in 2021 |CAS: 79-07-2

The Article related to danio embryos liver cancer chloroacetamide herbicides genotoxicity, acetochlor, apoptosis, chloroacetamide herbicide, embryo toxicity, reactive oxygen species, zebrafish, Toxicology: Agrochemical and other aspects.Electric Literature of 79-07-2

On June 30, 2021, Ma, Xinyan; Zhang, Ying; Guan, Mingyang; Zhang, Weidong; Tian, Huifang; Jiang, Caixiao; Tan, Xiaoxin; Kang, Weijun published an article.Electric Literature of 79-07-2 The title of the article was Genotoxicity of chloroacetamide herbicides and their metabolites in vitro and in vivo. And the article contained the following:

The toxicity of chloroacetamide herbicide in embryo development remains unclear. Acetochlor (AC) is a chloroacetamide that metabolizes into 2-ethyl-6-methyl-2-chloroacetanilide (CMEPA) and 6-ethyl-o-toluidine (MEA). The present study determined the potential effect of AC and its metabolites on embryo development. Both HepG2 cells and zebrafish embryos were exposed to AC, CMEPA and MEA in the presence or absence of co treatment with anti reactive oxygen species (ROS) reagent N acetylcysteine. The generation of ROS, levels of superoxide dismutase (SOD) and glutathione (GSH) in HepG2 cells and lactate dehydrogenase (LDH) leakage from HepG2 cells were investigated. The effects of AC, CMEPA and MEA on DNA breakage, MAPK/ERK pathway activity, viability and apoptosis of HepG2 cells were examined by comet assay, western blotting, MTT assay and flow cytometry, resp. Levels of LDH, SOD and GSH in zebrafish embryos exposed to AC, CMEPA and MEA were measured. The hatching and survival rates of zebrafish embryos exposed to AC, CMEPA and MEA, were determined, and apoptosis of hatched fish was investigated using acridine orange staining. The present data showed AC, CMEPA and MEA induced generation of ROS and decreased levels of SOD and GSH in HepG2 cells, which in turn promoted DNA breakage and LDH leakage from cells, ultimately inhibiting cell viability and inducing apoptosis, as well as phosphorylation of JNK and P38. However, co treatment with N-acetylcysteine alleviated the pro apoptosis effect of AC and its metabolites. Moreover, exposure to AC, CMEPA and MEA lead to toxicity of zebrafish embryos with decreased SOD and GSH and increased LDH levels and cell apoptosis, ultimately decreasing the hatching and survival rates of zebrafish, all of which was attenuated by treatment with N-acetylcysteine. Therefore, AC and its metabolites (CMEPA and MEA) showed cytotoxicity and embryo development toxicity. The experimental process involved the reaction of 2-Chloroacetamide(cas: 79-07-2).Electric Literature of 79-07-2

The Article related to danio embryos liver cancer chloroacetamide herbicides genotoxicity, acetochlor, apoptosis, chloroacetamide herbicide, embryo toxicity, reactive oxygen species, zebrafish, Toxicology: Agrochemical and other aspects.Electric Literature of 79-07-2

Referemce:
Amide – Wikipedia,
Amide – an overview | ScienceDirect Topics