文献类型：期刊文献

英文题名：Exposure to emamectin benzoate confers cytotoxic effects on human molt-4 T-cells and possible ameliorative role of vitamin E and dithiothreitol

作者：Chen, Yongjun[1];Liu, Xuefeng[1];Yan, Dongmei[1];Xu, Jialin[1];Luan, Shaorong[2];Xiao, Ciying[3];Huang, Qingchun[1]

机构：[1]East China Univ Sci & Technol, Sch Pharm, Shanghai Key Lab Chem Biol, Shanghai, Peoples R China;[2]East China Univ Sci & Technol, Sch Chem & Mol Engn, Shanghai, Peoples R China;[3]East China Univ Sci & Technol, Sch Biochem Engn, Shanghai, Peoples R China

年份：2023

卷号：46

期号：3

起止页码：413

外文期刊名：DRUG AND CHEMICAL TOXICOLOGY

收录：;WOS:【SCI-EXPANDED(收录号:WOS:000767046300001)】；

基金：This work was supported by the Project of Innovation Action Plan of Shanghai Municipal Science & Technology Commission in China [21S11901400, 22N41900100].

语种：英文

外文关键词：Emamectin benzoate; lymphocyte toxicity; oxidative stress; NF-kappa B signaling pathway; Molt-4 T-cells

摘要：Emamectin benzoate (EMB) is an avermectin insecticide that is extensively used for pest control, but there are few reports concerning its cytotoxic effects on human lymphocytes. In the current study, the hematotoxicity of EMB was evaluated in Molt-4 T-cells, a human T-lymphoblastic cell line with high motility, and the role of vitamin E (VitE) and dithiothreitol (DTT) in attenuating EMB cytotoxicity was characterized. Exposure of Molt-4 cells to EMB decreased cell viability and proliferation, induced a loss of cell clusters, and significantly increased membrane collapse and chromatin condensation. Moreover, EMB significantly increased cell death and suppressed transglutaminase activity. EMB treatment modulated the NF-kappa B signaling pathway, decreased the expression of p105, p50, and p65/ReIA in cytosolic and nuclear fractions, and increased nuclear I kappa B alpha expression. EMB increased oxidative stress, as demonstrated by a significant increase in the levels of reactive oxygen species (ROS). Treatment with noncytotoxic concentrations of VitE or DTT ameliorated the hematotoxicity induced by pretreatment with EMB, increased Molt-4 cell viability, raised the IC50 values of EMB, limited intracellular ROS generation, and mitigated EMB-mediated effects on NF-kappa B signaling. The results indicate the potential cytotoxicity of EMB on human lymphocytes, and demonstrate that VitE and DTT treatment can reduce the cytotoxic effects of EMB.