PubMed · 7212776
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B J Vermeer, F C Reman. 1980. Cholesterolester accumulation.. https://doi.org/10.1007/bf00404296
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During the 3-day period of the Los Angeles riots in 1992, there was a significant increase in the total number of deaths investigated by the Coroner's office and deaths attributed to violence and trauma, but not to atherosclerotic cardiovascular mortality. However, there was a significant decrease in cardiovascular mortality in the period following the riots, compared with the period of the riots or the preceding period.
NO and NO-donors are able to inhibit the peroxidation of polyunsaturated fatty acids in human low-density lipoproteins (LDL) exposed to Cu+2. Here we report that 1-hydroxy-2-oxo-3,3-bis(3-aminoethyl)-1-triazene (NOC-18), a compound which releases NO at low rate in aqueous solutions, powerfully inhibits the peroxidation of polyunsaturated fatty acids, tryptophan loss, the formation of fluorescent aldehydic adducts in apo B100 and the increase of electrophoretic mobility in isolated LDL undergoing oxidation. The inhibitory effect is not restricted to Cu+2-induced peroxidation but is also detectable with other oxidizing conditions such as the free radical generator 2,2'-azobis-(2-amidino propane) hydrochloride (AAPH), the combination of horseradish peroxidase and H2O2 (HRP), and peroxynitrite (ONOO-). The recognition of Cu+2-, AAPH-, and ONOO(-)-modified LDL by specific autoantibodies present in serum of atherosclerotic patients is almost completely inhibited when the oxidation procedure is performed in the presence of NOC-18. However, NOC-18 is completely ineffective in preventing the formation of recognizable antigens in HRP-modified LDL. These findings suggest that NO may efficiently prevent the formation of some, but not all, the antigenic epitopes recognized by human autoantibodies and thus likely formed during in vivo LDL oxidation.
The oxidation of low density lipoprotein (LDL) within atherosclerotic lesions may be involved in atherogenesis. LDL oxidation by cells in the presence of iron is faster at acidic pH. In addition, LDL oxidation by iron alone or iron cysteine in the absence of cells is much faster at acidic pH, even at mildly acidic pH (pH 6.5). The effect of pH on LDL oxidation by copper ions is more complex, in that acidity slows down the initial oxidation, as measured by conjugated dienes, hydroperoxides and thiobarbituric acid-reactive substances, but can increase the later stages of LDL oxidation as measured by increased macrophage uptake. Extensive LDL oxidation by cells in atherosclerotic lesions probably requires a source of iron or copper as catalysts for the oxidation. Iron in plasma is carried by the protein transferrin. Lowering the pH releases some of the iron from transferrin so that it can catalyse LDL oxidation. Copper is carried in plasma on caeruloplasmin and becomes more effective in catalysing LDL oxidation when the caeruloplasmin is preincubated at acidic pH, or even at pH 7.0. These effects can be seen with concentrations of caeruloplasmin and transferrin below those present in plasma. By analogy to other inflammatory and ischaemic sites, atherosclerotic lesions may well have an acidic extracellular pH, particularly within clusters of macrophages where the oxidative stress may also be high. This localised acidic pH may help to explain why atherosclerotic lesions are one of the few sites in the body where extensive LDL oxidation occurs.