الفهرس 
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Abstract
Many diseases including lung cancer and cardiovascular disorders have been attributed to the toxic effect of smoking. Smoking damages the vasculature particularly causing atherosclerotic lesions in the abdominal aorta and its distal branches. Consequently smoking is the most potent risk factor for the development of peripheral vascular disease. Smoking might be associated with endothelial dysfunction as an early event in atherogenesis. Cigarette smoke is known to contain a large number of free radicals, and it has been hypothesized that many of adverse effects of smoking may result from oxidative damage to critical biological substance.
Attention has focused on families of free radical catalyzed isomers of arachidonic acid, the isoprostanes, stable products of lipid peroxidation that circulate in human plasma and are excreted in urine.
One of the most abundant F2-isoprostanes produced in vivo is 8-epi-PGF2α , it is chemically stable and remain in the circulation until it is cleared by the kidney and can be estimated in the urine, 8-epi-PGF2α is a potent vasoconstrictor and serves as a marker of lipid peroxidation and in turn of oxidative stress. The present study aims to evaluate and correlate the effects of active smoking on urinary 8-epi-PGF2α and cotinine, in addition to serum nitric oxide in heavy, moderate and mild male smokers.
20 heavy-smokers, 20 moderate-smokers, 20 mild-smokers and 20 controls, were the materials of the present study. All subjects were healthy and were not receiving current medications, nutritional or antioxidant supplements.
Urinary 8-epi-PGF2α and cotinine were determined, in addition to serum nitric oxide in all groups.
Results of the present study revealed significantly increase in urinary 8-epi-PGF2α in smokers compared with those of control subjects, also the results revealed significantly increase in 8-epi-PGF2α in heavy-smokers compared with those of moderate-smokers. These results indicate that smokers are subjected to oxidative stress. Also the present study showed that heavy-smokers had significantly higher urinary cotinine concentrations on comparing with control subjects.
In active-smokers urinary 8-epi-PGF2α were positively significantly correlated with urinary cotinine. As well as, a dose response relationship was observed between the number of cigarettes smoked and both urinary cotinine & urinary 8-epi-PGF2α in the present work.
Our results revealed significant decrease in serum nitric oxide concentration in heavy-smokers compared with those of control subjects. Therefore, we can conclude that the primary vasodilator produced by endothelial cells, is affected in smokers, and this is probably responsible for the alteration of endothelium-dependent vasodilatation. This loss of endothelium-dependent relaxation is probably the first manifestation of injury to the endothelium caused by smoking, with such endothelial dysfunction being the forerunner of atherosclerosis.
It may be said that urinary 8-epi-PGF2α and serum nitric oxide are markers of oxidative stress which might give more accurate information about ROS which play an important role in pathogenesis of many diseases affecting the physiological functions of body systems. Detection of these markers is a non-invasive method that may become a useful surrogate in assessing the predisposition to atherosclerosis in smokers.
Our findings evidenced that concentration of 8-epi-PGF2α and cotinine in the urine as well as NO in the sera of smokers may be of great significance as an early predictor of complications associated with increased oxidative stress in smokers such as atherosclerosis.