Nitric oxide donor compounds inhibit the toxicity of oxidized low‐density lipoprotein to endothelial cells

FEBS Letters

Thomas, James P.¹  Kalyanaraman, B.²  Struck, Andrew T.²  Hogg, Neil² 

[1] Department of Biochemistry, Medical college of Wisconsin, Milwaukee, WI 53226, USA;Biophysics Research Institute, Medical College of Wisconsin, 8701 Watertown Plank Road, Milwaukee, WI 53226, USA

关键词: Nitric oxide;    Low-density lipoprotein;    Endothelial cell;    Toxicity;    Lipid peroxidation;    Atherosclerosis;   

DOI  :  10.1016/0014-5793(95)00178-C

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

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 μmol/l lipid hydroperoxide (LOOH). Selenium deficiency enhances the toxicity of LOOH such that 300 μmol/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.

【 授权许可】

Unknown