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SMOKING GUN
By Sean Henahan, Access Excellence SAN ANTONIO- While the link between smoking and heart disease has long been established. the pathogenic mechanisms have remained a mystery. It now appears the molecular missing link between cigarettes and the development of heart disease has been identified, reported researchers at the 35th Annual Conference on Cardiovascular Disease Epidemiology and Prevention. Researchers at the University of Southern California conducted a study involving 24 healthy African-Americans, half of whom were smokers and half were non-smokers. The researchers obtained blood samples and subjected the specimens to in vitro copper induced-oxidation. They measured the susceptibility of low-density lipoprotein (LDL, bad cholesterol) to oxidation using mass spectometry. The study revealed that LDL in the smokers was 40% more susceptible to oxidative modification than LDL in the non-smokers. These findings indicate that LDL from young adult smokers is more susceptible to oxidation and support the hypothesis that cigarette induced atherogenesis involves a lipoprotein oxidation pathway, said Dr. James Dwyer, University of Southern California School of Medicine. . There is now considerable evidence that LDL becomes far more dangerous when oxidized. Components of LDL, especially fatty acids, lose electrons when they interact with circulating free radicals. Once the LDL particles have been oxidized, they are no longer controlled by the blood vessels inherent lipid control mechanisms. "LDL receptors on cell membranes regulate the intake of cholesterol into cells. However, the normal receptors cannot recognize oxidized LDL. instead, those damaged LDL particles are recognized by entities called scavenger receptors in some cells," explained Dwyer. These scavenger receptors are found in the endothelial lining of the major blood vessels. Unlike the primary LDL receptors, these scavenger receptors do not stop absorbing LDL after reaching a certain level. The oxidized LDL accumulates in a type of macrophage called foam cells. The build up of high cholesterol foam cells literally clogs the arteries, beginning the process of atherosclerosis, resulting eventually in heart attack and stroke. Anti-oxidant process play a positive role in the body, countering the effects of free-radical; induced oxidation. A number of recent studies suggest that dietary and supplement forms of antioxidant vitamins, beta-carotene, vitamin C and vitamin E bolster the natural antioxidant effects, and reduce the susceptibility of LDL to oxidation. Studies are underway evaluating the interplay of oxidant and antioxidant process in smokers and non-smokers. Previous studies have also shown that cigarette smoking has a negative effect on the activities of high density lipoprotein, HDL, or good cholesterol. However, the observed effects were small and could not account fro the large impact of smoking observed in epidemiological studies. "But this very large effect of smoking on oxidative damage to LDL is consistent with a fairly large effect of smoking on the risk of heart disease," notes Dwyer. The current study is of great interest scientifically, says Dwyer, because it indicates a molecular mechanism by which smoking could initiate atherosclerosis or clot formation, increasing the risk of heart attack and stroke, he said. The next step will be to conduct larger studies to further evaluate the potential link between smoking, oxidation of LDL, and heart disease. For further discussion of oxidation, anti-oxidants, heart disease and cancer, please refer to the Newsmaker interview with Dr. Charles Hennekens. Transmitted: 95-03-12 16:00:57 EST
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Science Updates Index
