Oxidation macrophage oxidative attack

Oxidative Attack on Foreign Substances by the Body s Macrophages... 

Oxidative stress, which has been implicated in the pathogenesis of atherosclerosis,35-36 has been shown to considerably attack lipids, not only in LDL, but also in arterial macrophages.37-38 We have previously shown that lipid-peroxidized... 

The long-term influence of omega-3 fatty acid supplements is not known, and, for this reason, the American Heart Association has not recommended that supplements be taken (Krauss et al., 1996). There is a very real concern that dietary PUPAs of all types may enhance the accumulation of lipid oxidation products in lipoprotein particles, thus allowing the attack of lipid oxidation products on the pn>tein component of the LDL, the enhanced uptake of the damaged LDL by macrophages in the artery wall, and increased atherosclerosis (Allard ei ai, 1997 Felton ct si., 1994), (Monounsaturaled fatty acids are thought not to be involved in the oxidation scenario lead big to atherosclerosis.)... 

Atherosclerosis in humans can have severe clinical sequelae, including heart attack, stroke, and peripheral vascular disease. In developed countries, atherosclerosis is responsible for more morbidity and mortality than any other single degenerative disease. Research over the past few decades has led to a new consensus on the sequence of events that initiate atherosclerotic lesions. Many of these events, including the accumulation of cholesterol in macrophages ( foam cells ), are accelerated by low-density lipoprotein (LDL) that has undergone oxidative modification. The accumulation of lipoprotein cholesterol is clearly central to the initiation of the fatty streak — the first anatomically defined lesion in atherosclerosis. 

The main function of iNOS is the disabling of xenobiotics and tumor cells. NO released by macrophages and mast cells causes sufficient DNA damage in the attacked cells to induce apoptosis. The immunological potency of iNOS is further enhanced by the simultaneous release of substantial amounts of superoxide radicals, which cause oxidative damage. 

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