Objectives 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. Methods The initial study was conducted on 300 subjects; 138 of them were nonsmokers (62 men and 76 women) aged 14-72 years and 162 were current smokers (145 men and 17 women) aged 16-85 years. Uric acid, creatinine, and urinary cotinine were determined by the enzymatic colorimetric method and plasma thiocyanate by selective electrode. Results 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). Conclusion 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.

Aims:The aim of the present study was to investigate hyperhomocysteinemia in Tunisian bipolar I patients according to 5,10-methylenetetrahydrofolate reductase (MTHFR) C677T polymorphism. Methods:The subjects consisted of 92 patients with bipolar I disorder diagnosed according to DSM-IV, and 170 controls. Plasma total homocysteine, folate and vitamin B12 were measured. MTHFR C677T polymorphism was determined by polymerase chain reaction-restriction fragment length polymorphism.Results: Compared with controls, patients had a significantly higher homocysteine level (16.4 Ϯ 9.8 vs 9.6 Ϯ 4.5 mmol/L; P < 0.001) and a significantly lower folate level (3.2 Ϯ 0.9 vs 6.5 Ϯ 3.2 mg/L; P < 0.001). C677T MTHFR polymorphism genotype frequencies were in Hardy-Weinberg equilibrium. After adjustment for MTHFR C677T genotypes, hypofolatemia, hypovitamin B12 and for potential confounding factors, the odds ratio (OR) of hyperhomocysteinemia associated with bipolar disorder remained significant (OR, 5.53; 95% confidence interval: 1.92-15.86; P = 0.001). In patients, there was no significant change in hyperhomocysteinemia, hypofolatemia and hypovitamin B12 with regard to the clinical and therapeutic characteristics, whereas the highest prevalence of hyperhomocysteinemia was found in depressive patients and when illness duration was >12 years. Hypofolatemia was seen in all patients on lithium and in the majority of patients on carbamazepine, and the highest prevalence of hypovitamin B12 was noted in patients taking carbamazepine. Conclusion:Hyperhomocysteinemia was more frequent in bipolar I patients independent of C677T polymorphism. Patients had reduced levels of folate, which modulates homocysteine metabolism. Indeed, this finding indicates that folate supplementation may be appropriate for bipolar patients with hyperhomocysteinemia.

Cigarette smoking increases homocysteine, which is strongly correlated with cotininuria and plasma thiocyanates. Moreover, smokers had tendency to develop hypofolatemia and hypovitamin B12, particularly when the duration of consumption exceeded 20 years.

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