Quitting Smoking Raises Whole Blood Glutathione
Department of Psychiatry and Behavioral Sciences, Duke University Medical Center, Durham, NC 27710, USA. Physiology & Behavior
(Impact Factor: 2.98).
11/1996; 60(5):1379-81. DOI: 10.1016/S0031-9384(96)00328-9
Cigarette smoke contains numerous oxygen free radicals that may be important in smoking-related disease pathogenesis. These free radicals may overwhelm antioxidant defenses and produce a condition of oxidative stress that can result in damage to DNA and other cellular components. This study investigated whether or not indications of harmful oxidative stress decline following smoking cessation. Changes in whole blood glutathione (GSH), an index of oxidative stress level, were determined for 30 cigarette smokers who participated in an experimental smoking-cessation program. Measurements were taken during ad lib smoking and 3 weeks after smoking cessation. In 22 individuals who were continuously abstinent for 3 weeks, GSH levels rose significantly following smoking cessation, from 5.0 to 6.1 mumol/g Hb (p < 0.001). Individuals with the lowest GSH levels during ad lib smoking showed the greatest increases following cessation. Results suggest that oxidative stress and free-radical damage diminish soon after smoking cessation. Thus, some significant health benefits may appear rapidly when people quit smoking.
Available from: Nosratola D Vaziri
- "Conversely, high levels of total GSH in blood is found in healthy elderly subjects (Pastore et al. 2003). Oxidative stress caused by tobacco smoke has been reflected by lowered levels of whole blood GSH, which increases 3 weeks after smoking cessation (Lane et al. 1996). Likewise oxidative stress in chronic kidney disease is associated with reduced blood and tissue GSH levels (Vaziri 2004). "
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ABSTRACT: Chemical components of air pollutant exposures that induce oxidative stress and subsequent inflammation may be partly responsible for associations of cardiovascular morbidity and mortality with airborne particulate matter and combustion-related pollutant gasses. However, epidemiologic evidence regarding this is limited. An exposure-assessment approach is to measure the oxidative potential of particle mixtures because it is likely that hundreds of correlated chemicals are involved in overall effects of air pollution on health. Oxidative potential likely depends on particle composition and size distribution, especially ultrafine particle concentration, and on transition metals and certain semivolatile and volatile organic chemicals. For health effects, measuring systemic oxidative stress in the blood is one feasible approach, but there is no universal biomarker of oxidative stress and there are many potential target molecules (lipids, proteins, DNA, nitric oxide, etc.), which may be more or less suitable for specific study goals. Concurrent with the measurement of oxidative stress, it is important to measure gene and/or protein expression of endogenous antioxidant enzymes because they can modify relations between oxidative stress biomarkers and air pollutants. Conversely, the expression and activities of these enzymes are modified by oxidative stress. This interplay will likely determine the observed effects of air pollutants on systemic inflammatory and thrombotic mediators and related clinical outcomes. Studies are needed to assess the reliability and validity of oxidative stress biomarkers, evaluate differences in associations between oxidative stress biomarkers and various pollutant measurements (mass, chemical components, and oxidative potential), and evaluate impacts of antioxidant responses on these relations.
Air Quality Atmosphere & Health 03/2011; 4(1):37-52. DOI:10.1007/s11869-010-0095-2 · 1.80 Impact Factor
Available from: Jeffrey K Yao
- "Oxidative stress and free radical-induced damage diminishes soon after smoking cessation . Smoking cessation is associated with increase in GSH levels, observed within weeks after a person stops smoking, which in turn may be associated with improvement in risk factors for pulmonary and cardiovascular diseases . Erythrocytes of smokers show a greater susceptibility to hydrogen-peroxide-induced peroxidation than those of non-smokers before supplementation with vitamin E . "
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ABSTRACT: There is accumulating evidence of reductions in red blood cell membrane essential fatty acids in patients with schizophrenia. The mechanisms that may underlie these reductions have yet to be determined. It is possible that the observed membrane fatty acid deficits are associated with the development of schizophrenia. Alternatively, the membrane fatty acid deficits may be due to environmental factors, such as smoking and variations in diet, which may not be associated specifically with the pathophysiology of schizophrenia. Patients with schizophrenia smoke cigarettes at very high rates. Cigarette smoke contains many pro-oxidants that contribute directly to oxidative stress. Polyunsaturated fatty acids (PUFAs) are very susceptible to oxidative effects of free radicals. Thus, smoke-induced oxidative stress could plausibly account for reductions in membrane fatty acid in schizophrenia. Recent studies provide conflicting evidence for smoking effects on membrane fatty acid deficits. Likewise, the effects of diet on membrane PUFAs in schizophrenia are not entirely clear. Essential PUFAs need to be consumed in diet. Thus, differences in membrane PUFAs observed between patients and control subjects may be due to dietary variation. Few studies that have examined dietary effects differ in their interpretation of the effects of diet on membrane PUFAs. Thus, the jury is still out whether smoking or dietary effects are the primary causes of membrane PUFA deficits in patients with schizophrenia. Future studies will need to systematically examine the potential effects of smoking and diet, as well as other environmental factors such exercise, to definitively establish whether or not PUFA abnormalities are inherent to schizophrenia.
Prostaglandins Leukotrienes and Essential Fatty Acids 01/2004; 69(6):385-91. DOI:10.1016/j.plefa.2003.08.009 · 2.35 Impact Factor
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ABSTRACT: Our current concept of the etiology of atherosclerosis is that it is a chronic inflammatory process. In support of this model
serum markers of inflammation, such as high levels of C-reactive protein and fibrinogen, have been observed in numerous studies
to be sensitive predictors of future cardiovascular adverse events. These markers are a group of serum proteins that are termed
“acute phase reactants.” Their serum levels increase in the presence of any inflammatory process, the most common of which
are infections. And indeed it has been suggested that atherosclerosis may be due to a focus of infection, such as periodontal
disease. The infection then presumably spreads to the vascular tissues to initiate a local inflammatory process. Against this
model it has been found in clinical trials that antibiotics do not prevent adverse vascular events. Furthermore, agents, such
as statins, which have no antibacterial activity, have been shown in innumerable studies to be highly effective in the reduction
of number of vascular events occuring in a vulnerable population. The apparent association between periodontal and vascular
disease may be due to the fact that both conditions are much more common in smokers.
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