Cigarette Smoke Oxidation of Human Plasma Constituents (original) (raw)
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Oxidative stress in mouse plasma and lungs induced by cigarette smoke and lipopolysaccharide
Environmental Research, 2008
Short-term exposure to cigarette smoke (CS) or lipopolysaccharide (LPS) leads to acute lung inflammation through oxidant-antioxidant imbalance. We studied the response in mice exposed to smoke or LPS during five consecutive days, as measured by superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activities, as well as lipid peroxidation and nitric oxide levels in bronchoalveolar lavage fluid (BALF), lung homogenates, and plasma. Control mice were exposed to ambient air. Exposure to CS or LPS led to a similar influx of alveolar macrophages and neutrophils into the BALF; however, hydroxyproline levels were increased only in the CS group (p<0.001); SOD activity was increased in the BALF (p<0.001) and lung homogenates (p<0.05) of the CS group but was decreased in the BALF (p<0.05), lung homogenates (p<0.05) and plasma (p<0.01) of the LPS group. CAT activity was increased in the BALF (p<0.01), lung homogenates (p<0.001) and plasma (p<0.05) of the CS group but decreased in the BALF (p<0.001) and plasma (p<0.05) of the LPS group. GPx activity was reduced in the BALF (p<0.01) and plasma (p<0.01) of both the CS and LPS groups. Lipid peroxidation was increased in the BALF (p<0.001) and lung homogenates (p<0.001) of the CS group. Finally, the levels of nitrite were reduced in the CS (p<0.01) and LPS (p<0.001) groups. Our data show that the activity profiles of enzymes contributing to oxidant-antioxidant imbalance in the lungs differ depending on the inflammatory stimulus, and that SOD, CAT and GPx may be useful markers of oxidative stress in acute lung inflammation induced by exposure to CS.
Effect In Vivo of Cigarette Smoke on Lipid Peroxidation and Antioxidant status in Male albino Mice
Cigarette smoke (CS) contains free radicals that are considered to be a major group of carcinogens. Wistar mice were exposed to cigarette smoke for 16 weeks, 2cigarettes for 15 min/ twice daily, 6 days/wk. The control animals (C) inhaled clean room air. Biochemical markers in blood and lung tissues were analyzed. There was gradual increase in the lipid peroxidation indicated by augmented levels of thiobarbituric acid reacting substances (TBARS) in the lung tissue of cigarette smoke exposed animals when compared with that of control group. The enzymatic antioxidant levels such as superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX) were decreased significantly in CS exposed animals. The activity level of glutathione-S-transferase (GST) was increased in CS group when compared with that of control. The Non- enzymatic antioxidants such as vitamin-C and vitamin- E were decreased significantly in the serum of CS exposed mice. These results revealed that chronic expo...
Atherosclerosis, 2001
Epidemiological studies have shown that cigarette smoking is a major cause of atherosclerosis. Oxidants as well as nicotine in cigarette smoke have been implicated in atherogenesis. To clarify the mechanism involved, we examined the chronic effects of nicotine and nicotine-free cigarette smoke extracts (CSE) on oxidative modification of low-density lipoprotein (LDL) in the plasma of Watanabe heritable hyperlipidemic rabbits and atherogenesis in the aorta. CSE was prepared by bubbling the gas phase of smoke (1 ml/three cigarettes) into phosphate buffer saline, and 3 ml of this CSE was injected daily into the ear vein of the rabbit for five months. The rabbits treated with CSE showed an increase in lipid peroxide levels, estimated as thiobarbituric acid reactive substances (TBARS), with a corresponding decrease in vitamin E levels in the plasma. They also showed enhanced oxidative modification of LDL, assessed by anion-exchange HPLC, incorporation into macrophages and measurement of TBARS. These events could be efficiently prevented by administering vitamin E (150 mg/kg/day, p.o.). Nicotine alone (0.5 mg/kg/day, s.c.) led to a temporary increase in the plasma triglyceride level. At the end of the experiment, CSE but not nicotine had caused progression of atherosclerotic lesions together with accumulation of cholesteryl ester in the thoracic aorta, while vitamin E had significantly prevented such atheromatous formation. These results indicate that oxidants in CSE can promote the development of atherosclerosis through oxidative modification of plasma LDL, particularly in hypercholesterolemia, and offer evidence for increased vitamin E utilization in 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
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.
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.
Arteriosclerosis, Thrombosis, and Vascular Biology, 2004
Objective-Endothelial dysfunction is an early manifestation of cigarette smoke (CS) toxicity. We have previously demonstrated that CS impairs nitric oxide (NO)-mediated endothelial function via increased generation of superoxide anion (O 2 . ). In these studies, we investigated whether stable compounds present in CS activate specific pathways responsible for the increased endothelial O 2 . production.
CIGARETTE SMOKING AND THE OXIDATIVE STRESS INDUCED BIOCHEMICAL CHANGES
2023
An investigation was carried out to assess the health status of cigarette smokers, oxidative stress induced changes and prevalence of smoking among smokers of different age groups in Thiruvananthapuram city, situated in the southern part of Kerala, India. The 52 male volunteers, aged between 20 and 70 years who are residents in Ulloor ward of Thiruvananthapuram Corporation in Kerala state were selected for the study. Among these 52 subjects, 36 were current smokers and 16 were non-smokers. The body weight, height and duplicate blood pressure measurements at rest were taken. Fasting blood samples were collected to determine the changes in serum biochemical parameters like total cholesterol, malondialdehyde, sodium, potassium and selected heavy metals in smokers and non-smokers. Analysis of the results show that among the total participants, 69 % were smokers and of these smokers, 41.7 % were in the age group 36-50 years. The body weight of the smokers was found to be less than that of the nonsmokers in the same age group. The BMI of 72.2% smokers were found to be less than that of the non-smokers. 77.8 % of the smokers in the study population were hypertensive and the blood pressure increases with age. Serum total cholesterol levels in smokers were found to be higher than that of non-smokers and this excess cholesterol may get deposited in the blood vessels and causes atherosclerosis. The smokers with BMI less than 25 recorded highest cholesterol levels. Serum sodium and potassium levels in smokers were higher than that of non-smokers. The increase in serum sodium content in smokers was highly significant compared to non-smokers. Concentrations of serum malondialdehyde, the lipid peroxidation product and the heavy metals like Cu and Cd were also found to be significantly high in smokers. The studyproves that smoking enhances free radical production which results in the formation of lipid peroxidation products and degradation of macromolecules, which may lead to cell damage or death. Results of this study also indicate that there is a positive correlation between mean cadmium content and blood pressure of smokers.