Abstract
The purpose of this study was to examine the effect of cigarette smoking on plasma uric acid concentration and to determine the correlation between this parameter and the biological tobacco markers, plasma thiocyanate and urinary cotinine. The initial study was conducted on 300 subjects; 138 of them were nonsmokers (62 men and 76 women) aged 14-72years and 162 were current smokers (145 men and 17 women) aged 16-85years. Uric acid, creatinine, and urinary cotinine were determined by the enzymatic colorimetric method and plasma thiocyanate by selective electrode. Plasma uric acid concentration was significantly lower in smokers than in nonsmokers. A statistically significant negative correlation was noted between the smoking status parameters, including both the number of cigarettes smoked/day (F (3-161)=12.063; r=-0.9968; p=0.0001) and the duration of smoking (F (3-161)=1.305; r=-0.9406; p=0.0274), and the plasma uric acid. Among smokers, we noted a negative correlation between uric acid and both plasma thiocyanates (r=-0.437; p<0.05) and urinary cotinine (r=-0.580; p<0.05). After excluding the other factors affecting the uric acid levels, the significant low plasma uric acid in smokers was attributed to a reduction of the endogenous production as a result of the chronic exposure to cigarette smoke that is a significant source of oxidative stress. Therefore, it is recommended to stop or reduce smoking and to introduce plasma uric acid estimation as a routine test, since it is cheap and simple to reflect the antioxidant level.
Highlights
Cigarette smoking is known to contribute to many diseases, including cancer, chronic obstructive pulmonary disease, stroke, cardiovascular diseases, and peptic ulcers [1, 2]
A statistically significant negative correlation was noted between the smoking status parameters, including both the number of cigarettes smoked/day (F3–161 = 12.063; r = -0.9968; p = 0.0001) and the duration of smoking (F3–161 = 1.305; r = -0.9406; p = 0.0274), and the plasma uric acid
We noted a negative correlation between uric acid and both plasma thiocyanates (r = -0.437; p \ 0.05) and urinary cotinine (r = -0.580; p \ 0.05)
Summary
Cigarette smoking is known to contribute to many diseases, including cancer, chronic obstructive pulmonary disease, stroke, cardiovascular diseases, and peptic ulcers [1, 2]. Investigators have attempted to elucidate the mechanisms of the pathogenesis associated with cigarette smoking, but the conclusions were not consistent. A basic hypothesis is that free radicals cause oxidative damage to macromolecules such as lipids, proteins, and DNA. These radicals play an important role in the pathogenesis of diseases [3]. In accordance with this theory, antioxidants are believed to play important roles in resisting damage from oxidative stress resulting from cigarette smoking.
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