Changes in the Antioxidant Defense System of the Smokers # (original) (raw)
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Evaluation of Antioxidant Status in Passive Smokers
Chronic exposure of human body to tobacco smoke environment induces oxidative stress in cells as a consequence of oxidative reactions by increasing the production of oxygen-free radicals. The aim of this study is to evaluate the influence of passive smoking on antioxidant status in adults. in accordance with their physiological role, erythrocytes are continuously exposed to oxidative stress. Analysis of oxidative susceptibility in the exposed erythrocytes to tobacco smoke was assessed by measurement of erythrocytic superoxide dismutase (sod) and glutathione-peroxidase, in 50 adult passive smokers, compared with non-smokers. in case of chronic exposures (more than 15 years) in environment with tobacco smoke, the results of erythrocytic superoxide dismutase indicates an adaptive response of the organism to the oxidative stress, which is considered to be antioxidantdefense response, induced by altering the gene expression of SOD from the stem cells. Significantly increasing of erythrocyte sod is associated with lower-level glutathione peroxidase activity in passive smokers compared to non-smokers. our research results reveal the fact that chronic exposure to tobacco smoke environment generates biochemical imbalance in erythrocytic antioxidant defense, providing a protective adaptive mechanism at cellular and sub-cellular levels.
Effect of Cigarette Smoking on the Oxidant/Antioxidant Balance in Healthy Subjects
American Journal of Therapeutics, 2007
Background and Purpose: Cigarette smoking has been associated with the development of cardiovascular disease and cancer. Even though the molecular mechanism(s) are not clear, the pathology has been related to oxygen free radicals present in cigarette smoke. Thus, the main objective of this study was to establish the changes in the oxidation/antioxidation balance induced by cigarette smoking.
Effects of Cigarette Smoking on Blood Antioxidant Status in Short-Term and Long-Term Smokers
DergiPark (Istanbul University), 2001
To determine the effects of cigarette smoking on blood antioxidant status and lipid peroxidation, 16 healthy male current smokers (CS) and 16 healthy male non-smokers (NS) serving as controls were studied. CS were divided into two groups: short-term smokers (STS) 35.4 ± 5.8 years of age (mean±SD), and long-term smokers (LTS) 60.9 ± 4.9 years of age. The average smoking period of STS and LTS were 8.1 ± 1.1 years (mean ±SD) and 20.5 ± 4.5 years (mean ± SD)respectively. STS and LTS had their own controls, who were NS (young NS and old NS respectively). It was concluded that the changes in the enzymatic and nonenzymatic antioxidant defense systems of elderly smokers may be due to oxidative stress caused by cigarette smoking.
Polskie Archiwum Medycyny Wewnętrznej, 2008
Exposure to tobacco smoke is an extremely important risk factor determining the development of respiratory diseases, cardiovascular diseases and cancer. Passive exposure is common and often not realized by the exposed subjects. Markers of tobacco smoke exposure are nicotine metabolites, i.e. cotinine and trans-3'-hydroxycotinine. The objective of the study was to assess the level of passive exposure to tobacco smoke among students and the exposure impact on the blood hemoglobin level, peak expiratory flow (PEF), lipid peroxidation level and antioxidant enzyme activity. A total of 104 subjects were enrolled in the study. The subjects were categorized in 3 subgroups depending on nicotine metabolite levels in blood (subgroup I with metabolite level > 100 ng/ml (high exposure); subgroup II with the metabolite level of 10-100 ng/ml; subgroup III with metabolite level <10 ng/ml). The blood hemoglobin level, PEF, levels of lipid peroxidation metabolites--malondialdehyde and 4-hyd...
The Total Antioxidant Status in Cigarette Smoking Individuals
Active smokers are exposed to reactive free radicals that are present in cigarette smoke. Oxygen free radicals, including superoxide, hydroxyl radicals, peroxyl radical hydrogen peroxide and singlet oxygen, are highly reactive species that can cause a wide spectrum of cell damage including enzyme inactivation, lipid peroxidation, protein and lipoprotein oxidation, and DNA damage. Free radicals are believed to be involved in the pathogenesis of cardiovascular diseases and cancer. The purpose of the present study was to measure the total antioxidant status (TAS) in active cigarette smoking individuals in Mosul city. Twenty active smokers and twenty nonsmokers participated1in the study. Blood sample was taken from each individual and the TAS had been measured in the sera using the Cayman chemical antioxidant assay kit (USA). The results obtained from the study revealed a significant (P<0.001) reduction of the TAS in the smoker's group as compared with the non-smoker's group. In conclusion, smokers possess low TAS than non smokers which may be due to the presence of high amounts of free radicals in cigarette smoke that generate an oxidative stress in the smoker's body that may cause exhaustion of antioxidants of the body.
Effects of Active and Passive Smoking on Antioxidant Enzymes and Antioxidant Micronutrients
Biotechnology & Biotechnological Equipment, 2005
In the present study, we analyzed the relationship between cigarette smoke exposure and several markers of oxidative status, plasma thiobarbituric acid reactive substances, erythrocyte glutathione peroxidase, superoxide dismutase and catalase in a group of students. Of the 105 men enrolled into the study, 35 had never smoked and not exposed to cigarette smoke at all. Thirty five had smoked at least 15 cigarettes per day for at least five years (active smokers) and 35 had been exposed to cigarette smoke at indoor environment at least 2 cigarette/day on ≥5d/wk for > 6 months (passive smokers). The urine cotinine level was used as a smoking marker. Erythrocyte SOD activity and plasma TBARs were significantly higher in active and passive smokers than in non-smokers (p < 0.05). However, erythrocyte GSH-Px and CAT were significanly lower in active smokers than in non smokers (p < 0.05). Serum vitamin C and E levels were significantly lower in active and passive smokers than in nonsmokers (p < 0.05). For active and passive smokers, there were significant possitive correlations between urine cotinine levels and plasma TBARs levels (r = 0.60, p < 0.01, r = 0.43, p < 0.05) and a negative correlation between urine cotinine levels and plasma vitamin C (r = -0.48, p < 0.05, r = -0.59, p < 0.01). In conclusion, during both passive and active smoking, oxidative stress was clearly exacerbated and the dynamic balance between oxidation and antioxidation was seriously disrupted, which was closely related to many disorders or diseases in active and passive smokers.
Effect of cigarette smoking on the oxidation/antioxidation balance in healthy subjects
Revista Latinoamericana de Hipertension
Background and Purpose Cigarette smoking has been associated with the development of cardiovascular disease and cancer. Even though the molecular mechanism is not clear yet, it has been related to the oxygen free radicals. Thus, the main objective of this study was to establish the changes in the oxidation/antioxidation balance induced by cigarette smoking. Methods 30 healthy subjects (15 smokers and 15 non smokers) of both genders were studied. The smokers group had smoked a mean of 14 cigarettes per day during 4.5 years. Fasting serum levels of malondialdehyde (MDA), nitric oxide (NO), reduced glutathione (GSH) and vitamin C (ascorbic and dehydroascorbic acid) were measured. Results Fasting NO concentration was significantly higher in smokers (51.3 ± 5.3 µM) than non-smokers (35.2 ± 4.8 µM, p
ABSTRACT Background: Oxidative stress plays an important role in the pathogenesis of some diseases such as lung cancer, chronic obstructive pulmonary disease, and atherosclerosis. 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. Aim: The present study was conducted to determine the effect of cigarette smoking on changes in lipid peroxidation and antioxidant status in cigarette smokers. Materials & Methods: The study population consisted of 150 male subjects divided into two groups; 88 smokers and age- and sex-matched non-smokers 62 subjects were selected. Biochemical parameters such as lipid peroxidation thiobarbituric acid reactive substances malondialdehyde (MDA) and antioxidants (superoxide dismutase (SOD),catalase (CAT), reduced glutathione (GSH), vitamin A, vitamin C and vitamin E were measured by colorimetric methods. Results: Enhanced lipid peroxidation with...
Adult Healthy Smokers; Lipid Peroxidant and Antioxidant Activity
The professional medical journal, 2016
from December 2013-July 2014. Subjects and Methods: 77 smokers and 50 healthy controls were selected through non-probability purposive sampling. Blood glucose, lipids, MDA, antioxidant enzymes (SOD & GPX), serum bilirubin and uric acid (UA) were measured. Data was analyzed on Statistic software 8.1 by student's t test and Chi square test. The significant p-value was taken at ≤ 0.05. Results: Anti-oxidant enzymes (SOD & GPX), blood lipids, lipid per oxidant marker; the MDA, bilirubin and UA showed statistically significant differences between smokers and controls (p<0.001). Total blood lipids and lipid sub fractions were elevated in smokers. MDA in smokers was 3.17±0.91 µmol/ml compared to 1.15±0.61 µmol/ml (p=0.001) in controls. Smokers showed reduced SOD, GPX, serum bilirubin and UA, was significant (p=0.0001) in comparison to controls. Conclusion: Cigarette smoke is a significant source of oxidative stress. Smoking increases malondialdehyde and reduces superoxide dismutase, glutathione peroxidase, uric acid and bilirubin.
Alterations of small-molecular-weight antioxidants in the blood of smokers
Chemico-Biological Interactions, 1998
Plasma h-tocopherol, ascorbate, retinol, uric acid, and lipid peroxides were investigated in 39 male smokers and 64 male non-smokers. The average level of plasma h-tocopherol of 35-45-year-old smokers (1.74 90.49 vg/mg total lipid) was significantly lower than that of age-matched non-smokers (2.55 90.88 vg/mg total lipid, P= 0.032). Similarly, the plasma h-tocopherol of smokers aged above 45 (1.66 9 0.29 vg/mg total lipid) was lower than that of the age-matched non-smokers (2.389 1.26 vg/mg total lipid, P= 0.014). However, no difference in plasma level of h-tocopherol was found between smokers and non-smokers below the age of 35. The average concentration of ascorbate in plasma was significantly decreased only in those smokers older than 45 (0.33 9 0.16 mg/dl vs non-smokers 0.53 9 0.19 mg/dl, P= 0.003). The average level of lipid peroxides (measured as malondialdehyde, (98)00083-0 C.S. Liu et al. / Chemico-Biological Interactions 116 (1998) 143-154 144 MDA) in the plasma of smokers (2.77 9 0.51 nmol/ml) was higher than that of nonsmokers (2.35 90.21 nmol/ml) aged above 45 (P= 0.034). No differences in the plasma levels of uric acid and retinol were noted between smokers and non-smokers in all age groups. Using partial correlation analysis under age control, we found that the plasma level of h-tocopherol was negatively correlated with the plasma level of MDA (r= − 0.523, P =0.038). In contrast, the plasma level of ascorbate was only weakly correlated with the plasma level of MDA (r= −0.341, P= 0.094). Moreover, we found a negative correlation between the plasma level of h-tocopherol and smoking index (r= −0.414, P =0.006) under age control, but there was no correlation between plasma level of ascorbate and smoking index (r= 0.221, P= 0.193). These results indicate that adequate levels of h-tocopherol and ascorbate may protect the plasma from oxidative damage elicited by smoking-mediated reactive oxygen species (ROS) and free radicals in young smokers. However, the antioxidant activities of h-tocopherol and ascorbate may be overwhelmed by the long-standing oxidative stress elicited by cigarette smoking in elderly subjects.