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

Abstract:

: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.

journal_name

FEBS Lett

journal_title

FEBS letters

authors

Struck AT,Hogg N,Thomas JP,Kalyanaraman B

doi

10.1016/0014-5793(95)00178-c

subject

Has Abstract

pub_date

1995-03-20 00:00:00

pages

291-4

issue

2-3

eissn

0014-5793

issn

1873-3468

pii

0014-5793(95)00178-C

journal_volume

361

pub_type

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