Oxidative stress plays an important role in the pathogenesis of some diseases such as lung cancer, chronic obstructive pulmonary disease, and atheroscleorosis. Smoking may enhance oxidative stress not only through the production of reactive oxygen radicals in smoke but also through weakening of the antioxidant defense systems. In this study, we investigated the effects of smoking on lipid peroxidation and paraoxonase activity in a healthy population. The study consisted of (n = 30) smokers and (n = 30) nonsmokers. The age of the population which is studied was 44.74 +/- 10.59 yr. The levels of serum malondialdehyde (MDA) and paraoxonase (PON1) activities were measured by the modified Buege method and the Eckerson method, respectively. Student's t-test was used to analyze the data. The serum MDA levels were significantly higher (p < .05) and serum PON1 activities were significantly lower (p < .001) in smokers than in nonsmokers. Thus, increased levels of serum MDA and decreased PON1 activities may be important in determining the oxidant/antioxidant imbalance in smokers.

The spin-lattice relaxation rates (1/T1) of serum, whole blood, and red cells were measured vs several concentrations of transition metal ions. For comparative purposes, the similar experiments were repeated in water. The rates show a linear dependence on concentration of each ion for water, but nearly a linear dependence for blood and its constituents. The influence of each ion on 1/T1 in a sample was expressed by the slope (relaxivity) of the least-squares fitting of 1/T1 vs ion concentration. The relaxivities of Mn(II) in serum and of Fe(III) in serum and blood are greater than those in water, whereas the relaxivities of these ions in the other cases and of all the other ions in call cases are smaller than those in water. However, the relaxivity data show that Cr(III) in serum and blood affects the 1/T1 rates. The ratio of relaxivity of each sample to that of water is known as proton relaxation enhancement (PRR) factor (epsilon). The epsilon factors for present data suggest that the added ions are bound to proteins, and only Mn(II) in serum and Fe(III) in blood and serum are accessible to water.

ABSTRACT. An insertion/deletion (I/D) polymorphism was identified in intron 16 of the gene encoding the human angiotensin I-converting enzyme (ACE), a candidate gene for chronic obstructive pulmonary disease (COPD). We investigated the relationship between this polymorphism in the ACE gene and the risk of developing COPD. Sixty-six COPD in-patients and 40 non-smoking control individuals were recruited for this study. The distribution of ACE genotypes in these individuals was studied. The frequencies of ACE genotypes were found to be 47.0% for DD, 30.3% for ID, and 22.7% for II in the COPD group and 32.5% for DD, 47.5% for ID, and 20.0% for II in the control group. The allele frequencies were found to be 0.62% for the D allele and 0.38% for the I allele in the COPD group and 0.56% for the D allele and 0.44% for the I allele in the control group. A significant difference ACE gene and chronic obstructive pulmonary disease was found between I and D allele frequencies (P < 0.05) of the study and control groups. Our results suggest that this ACE polymorphism may be associated with the development of COPD.

No abstract

Abstract:Purpose: In the current study we aim to investigate the effects of vitamin C and profol on red blood cell deformability in diabetic rats Materials and methods: Twenty-eight Wistar Albino rats were included in the study after streptozocin (60 mg/ kg) treatment for 4 weeks of observation for diabetes presence. Twenty-eight rats were allocated to 4 groups. In group DP (n = 7) 150 mg.kg -1 of propofol was injected intraperitoneally. In group DP-vit C (n = 7) rats 100 mg/kg of vitamin C (Ascorbic acid, Redoxon ® 1000 mg/5 mL -Roche) were applied one hour before administrating 150 mg.kg -1 of propofol, while rats in control group (n = 7), and diabetic control group (n = 7) received intraperitoneally physiological saline. Deformability measurements were achieved by using erythrocyte suspensions with hematocrit level of 5 % in PBS buffer. Results: Erythrocyte deformability was signifi cantly higher in diabetic control group than in control and vitamin C plus propofol groups (p = 0.00, p = 0.025, respectively). Erythrocyte deformability indexes were found similar in control group and vitamin C plus propofol group (p = 0.949). Relative resistance was increased in diabetic rat model. Conclusions: Erythrocyte deformability was damaged in rats with diabetes. This injury might lead to further problems in microcirculation. Application of propofol did not alter red cell deformability in diabetic rats. Vitamin C supplementation seems to reverse those negative effects and variations in erythrocyte deformability (Fig. 2