Endosulfan inducing apoptosis and necroptosis through activation RIPK1 in human umbilical vascular e

• 作 者: LianshuangZhang;JialiuWei;LiJing;ManYang;JiWang;ZhiweiSun;XianqingZhou;
• 机 构: Department of Toxicology and Hygienic Chemistry, School of Public Health,Capital Medical University,
• 出 处: 第六届亚洲特大城市环境与公共健康论坛暨中国环境科学学会环境医学与健康分会2015年会
• 发表日期: 2015年期

　　Epidemiological studies have indicated that persistent organic pollutants (POPs) exposure is most likely relevant to atherosclerosis.Endosulfan was an organochlorine pesticide and extensively used in agriculture.In present study, human umbilical vein endothelial cells (HUVECs) were chosen as model cells to systematically explore the toxicity of endosulfan.The results indicated that exposure to endosulfan could inhibit proliferation, damage the cell membrane and induce the release of the inflammatory cytokines.The results showed that endosulfan up-regulated the expressions of RIPK1/Caspase8/Caspase3 and RIPK1/RIPK3/MLKL,which means the activation of RIPK1 pathways;and led to apoptosis and necroptosis..Furthermore, N-acetyl-L-cysteine (NAC) effectively antagonized some of the endosulfan-induced responses.The results demonstrated that endosulfan could induce the injury and dysfunction of HUVECs through the activation of RIPK1, which is associated with oxidative stress, suggesting that exposure to endosulfan may be a potential hazardous factor for early atherosclerosis.