The aim of this study was to test the hypothesis that allopurinol ingestion modifies the slow component of • VO2 kinetics and changes plasma oxidative stress markers during severe intensity exercise. Six recreationally active male subjects were randomly assigned to receive a single dose of allopurinol (300 mg) or a placebo in a double-blind, placebo-controlled crossover design, with at least 7 days washout period between the two conditions. Two hours following allopurinol or placebo intake, subjects completed a 6-min bout of cycle exercise with the power output corresponding to 75 % • VO2 max. Blood samples were taken prior to commencing the exercise and then 5 minutes upon completion. Allopurinol intake caused increase in resting xanthine and hypoxanthine plasma concentrations, however it did not affect the slow component of oxygen uptake during exercise. Exercise elevated plasma inosine, hypoxanthine, and xanthine. Moreover, exercise induced a decrease in total antioxidant status, and sulfhydryl groups. However, no interaction treatment x time has been observed. Short term severe intensity exercise induces oxidative stress, but xanthine oxidase inhibition does not modify either the kinetics of oxygen consumption or reactive oxygen species overproduction., R. A. Olek ... [et al.]., and Obsahuje seznam literatury
Periodontal disease is a common oral disease. Inflammatory and immune responses to oral microorganisms initiate the development of periodontitis. Cigarette smoking is an important environmental risk factor for periodontitis. Another important inflammatory mediator is nitric oxide (NO). NO modulates vascular tone, microvascular permeability, leukocyte migration and oxidative activity, contributing to the direct killing of microorganisms. Several polymorphisms of the NOS3 gene have been detected, which may alter gene expression and NO synthesis. The aim of this study was to examine the association between the NOS3 rs1799983 and rs2070744 polymorphisms and periodontal disease. This study enrolled 200 patients with periodontal diseases (130 were non-smokers and 70 were smokers) and 160 control subjects (126 were non-smokers and 34 were smokers). Among the patients with periodontal disease, we observed a statistically increased frequency of patients with the CT genotype (TC vs. TT; 95%CI 1.83, OR 1.16–2.88, P = 0.011). There was a statisti-cally significant increased frequency of CT genotype carriers among non-smoking patients with periodontal disease as compared with non-smoking controls, whereas there were no statistically significant differences between smoking patients with periodontal disease and smoking control subjects. The results of our study suggest an association between the NOS3rs2070744 polymorphism and periodontal disease. and Corresponding author: Andrzej Pawlik