A Water-Soluble Fullerene Vesicle Alleviates Angiotensin II-Induced Oxidative Stress in Human Umbilical Venous Endothelial Cells

Publisher Website
Google Scholar
Abstract
A water-soluble fullerene vesicle based on the Buckminsterfullerene molecule (Ph5C60K, denoted as PhK) was explored to determine its effects on anti-oxidation of human umbilical endothelial cells (HUVEC) exposed to exogenous and endogenous reactive oxygen species (ROS). Hydrogen peroxide 0.05−0.25 mmol/L remarkably reduced the cellular viability of HUVEC. This reduction in viability was markedly improved when PhK 0.01−1 μmol/L was added simultaneously to the culture medium. The reduction of viability in HUVEC induced by angiotensin II (AII) 10−9 to 10−7 mol/L was improved by pretreatment with PhK 0.1 or 10 μmol/L 12 h before AII stimulation. The ROS indicator CM-H2DCFDA demonstrated the efficacy of PhK 1 or 10 μmol/L in decreasing AII-induced ROS production to the level induced by the AII receptor blocker RNH-6470 20 μmol/L. The AII-induced peroxynitrite formation, as gauged using hydroxyphenyl fluorescein as a probe, was alleviated significantly by either pretreatment with PhK 0.1 or 1 μmol/L. Electron microscopy revealed intracellular localization of PhK in HUVEC after 12 h incubation. The PhK decreased the AII-induced apoptosis and lipid peroxidation processes as revealed by hexanoyl-lysine adduct formation. These observations show that the PhK water-soluble fullerene vesicle is promising as a compound controlling not only exogenous ROS, but also endogenous AII-mediated pathophysiological conditions. (Hypertens Res 2008; 31: 141−151)