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Journal of Lipid Research, Vol 36, 1756-1762, Copyright © 1995 by Lipid Research, Inc.
N Hogg, A Struck, SP Goss, N Santanam, J Joseph, S Parthasarathy and B Kalyanaraman
We have previously shown that nitric oxide donors inhibit the oxidation of
low density lipoprotein (LDL) initiated by copper ions or by azo-bis-
amidinopropane (Hogg et al., 1993. FEBS Lett. 334: 170-174). In this study,
the nitric oxide donors S-nitroso-N-acetylpenicillamine (SNAP), spermine
NONOate, and sodium nitroprusside were tested for their ability to inhibit
macrophage-dependent oxidation of LDL. SNAP and spermine NONOate inhibited
macrophage-dependent oxidation of LDL in a time- and
concentration-dependent manner. We propose that nitric oxide is acting as a
chain-breaking antioxidant that can inhibit the progression of lipid
peroxidation in cell dependent-oxidation of LDL. By this mechanism nitric
oxide could be an endogenous defense against atherogenesis. In contrast,
sodium nitroprusside enhanced cell-mediated oxidation of LDL by a mechanism
dependent on superoxide production and transition metal ions. Sodium
nitroprusside also enhanced LDL oxidation by cell culture medium alone by a
similar mechanism. The use of sodium nitroprusside as a nitric oxide donor
in cellular systems appears to be complicated by the release of iron
leading to an enhanced oxidative stress. Thus the effects of sodium
nitroprusside in such systems may be unrelated to nitric oxide release.
ARTICLES
Inhibition of macrophage-dependent low density lipoprotein oxidation by nitric-oxide donors
Biophysics Research Institute, Medical College of Wisconsin, Milwaukee 53226-0509, USA.
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