2, 3′, 4, 4′, 5-Pentachlorobiphenyl impairs insulin-induced NO production partly through excessive ROS production in endothelial cells. (13th October 2017)

• Record Type: Journal Article
• Authors: Long, Yang; Huang, Can; Wu, Jian; Cheng, Jin-nan; Liang, Guan-nan; Jiang, Chun-xia; Wan, Qin
• Is Part Of: Toxicology mechanisms and methods. Volume 27:Number 8(2017)
• Page Start: 592
• Page End: 597
• Publication Date: 2017-10-13
• Subjects: Polychlorinated biphenyls -- 2, 3′, 4, 4′, 5-pentachlorobiphenyl -- endothelial nitric oxide synthase -- nitric oxide -- ROS; Analytical toxicology -- Periodicals; Toxicology -- Periodicals; Toxicology -- Methodology -- Periodicals; 615.907
• DOI: 10.1080/15376516.2017.1337259
• Languages: English
• ISSNs: 1537-6516

Abstract

Abstract: Polychlorinated biphenyls (PCBs) have been reported to be associated with increased risk to hypertension, atherosclerosis, cardiovascular disease, etc. 2, 3′, 4, 4′, 5-Pentachlorobiphenyl, known as PCB-118, is a member of coplanar PCBs which renders their structure similar to polychlorinated dibenzo- p -dioxins (PCDDs) and has dioxin-like activity. In our current study, we investigated the effect of PCB-118 exposure on nitric oxide (NO) production and the underlying mechanisms in vitro . Exposure of PCB-118 impaired insulin-induced NO production and endothelial nitric oxide synthase (eNOS) activity in human umbilical vein endothelial cells (HUVECs) with no significant effect on cell viability. Furthermore, PCB-118 treatment induced oxidative stress. In addition, scavenging of reactive oxygen species (ROS) by 10 μM N -acetyl-l -cysteine (NAC) partly rescued impaired insulin-induced eNOS activities and NO productions induced by PCB-118 in HUVECs. Taken together, these results indicate that PCB-118 mediates lower eNOS activity and impairs insulin-induced NO production partly through excessive ROS production in endothelial cells.