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 Lettjournal_title
FEBS lettersauthors
Struck AT,Hogg N,Thomas JP,Kalyanaraman Bdoi
10.1016/0014-5793(95)00178-csubject
Has Abstractpub_date
1995-03-20 00:00:00pages
291-4issue
2-3eissn
0014-5793issn
1873-3468pii
0014-5793(95)00178-Cjournal_volume
361pub_type
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