Nitric oxide donor compounds inhibit the toxicity of oxidized low-density lipoprotein to endothelial cells. FEBS Lett 1995 Mar 20;361(2-3):291-4
Date
03/20/1995Pubmed ID
7698340DOI
10.1016/0014-5793(95)00178-cScopus ID
2-s2.0-0028956707 (requires institutional sign-in at Scopus site) 63 CitationsAbstract
Photo-oxidized low-density lipoprotein is cytotoxic to bovine aortic endothelial cells in a concentration-dependent manner. Total cell killing occurs at a concentration of 600 mumol/l lipid hydroperoxide (LOOH). Selenium deficiency enhances the toxicity of LOOH such that 300 mumol/l LOOH is cytotoxic. This toxicity is inhibited by desferrioxamine, a transition metal ion chelator, and by butylatedhydroxytoluene, a potent inhibitor of lipid peroxidation. Toxicity is also inhibited by the nitric oxide donors S-nitrosoglutathione and spermine NONOate but not by reduced or oxidized glutathione and spermine. We propose that nitric oxide, released from these compounds, is inhibiting the toxicity of LOOH to selenium-deficient endothelial cells. Furthermore we hypothesize that the mechanism for this inhibition of toxicity is the scavenging of the propagatory peroxyl and alkoxyl free radicals, by nitric oxide, that are generated during peroxidation of cell membranes.
Author List
Struck AT, Hogg N, Thomas JP, Kalyanaraman BAuthors
Neil Hogg PhD Associate Dean, Professor in the Biophysics department at Medical College of WisconsinBalaraman Kalyanaraman PhD Professor in the Biophysics department at Medical College of Wisconsin
James P. Thomas MD, PhD Professor in the Medicine department at Medical College of Wisconsin
MESH terms used to index this publication - Major topics in bold
AnimalsAorta, Thoracic
Butylated Hydroxytoluene
Cattle
Cell Survival
Deferoxamine
Dose-Response Relationship, Drug
Endothelium, Vascular
Glutathione
Glutathione Disulfide
Kinetics
Lipid Peroxides
Lipoproteins, LDL
Nitric Oxide
Nitroso Compounds
Platelet Aggregation Inhibitors
S-Nitrosoglutathione
Selenium
Spermine