Lipolysis in smokers during tobacco withdrawal: a pilot study

OBJECTIVE: Nicotine has an influence on several metabolic events, such as lipid metabolism. Habitual smoking increases plasma levels of glycerol as well as noradrenaline, which is the main stimulating hormone of adipose tissue lipolysis. However, the long-term effect of smoking on lipolysis is unclear. We compared nocturnal lipolysis in habitual smokers during short-term tobacco withdrawal with a control group of non-smokers. MATERIAL AND METHODS: Sixteen healthy subjects (9 heavy smokers and 7 non-smokers) were recruited in the study. The smokers were not permitted to smoke for at least 7 h before the test. The microdialysis technique was used to measure glycerol levels, the end-product of lipolysis, in subcutaneous adipose tissue. Variations in adipose tissue blood flow were measured using the ethanol technique. Glycerol, lactate and glucose concentrations as well as ethanol outflow/inflow ratio were measured between 2400 and 0600 h. RESULTS: There were no significant differences in subcutaneous glycerol or glucose concentrations between smokers and non-smokers. Between 0300 and 0600 h, lactate levels in smokers were lower than those in non-smokers. Adipose tissue blood flow did not differ between the groups. CONCLUSIONS: Despite potent acute and direct effects of smoking on lipolysis, we could not find any significant differences in basal lipolysis rate between smokers during short-term tobacco withdrawal and non-smokers.     

Smoking or its cessation does not alter the susceptibility to in vitro LDL oxidation

BACKGROUND: Enhanced induction of low density lipoprotein (LDL) oxidation may play a role in the increased cardiovascular risk in smokers. We determined LDL oxidisability in vitro in non-smokers, smokers and in subjects after smoking cessation. PATIENTS AND METHODS: Plasma lipids and copper induced LDL oxidation in vitro were measured in 31 persistent smokers, 47 smokers who tried to stop smoking and 25 non-smokers. In the smoking cessation group, blood was collected before then 1, 3, 6 and 12 months after smoking cessation, and in the persistent smoking and non-smoking groups at baseline and after 12 months. Plasma thiobarbituric acid reactive substances (TBARS) were measured 3 times (at baseline then after 1 and 3 months) in all subjects who refrained from smoking (controlled by urinary cotinine concentrations) for at least 3 months. RESULTS: At baseline, no differences in mean age, body mass index and lipid profiles between groups were present. Seventeen subjects of the smoking cessation group (36%) managed to quit during 12 months. Smoking cessation was associated with an increase in mean weight (P 相似文献   

Effects of cigarette smoking on the antioxidant defence in young healthy male volunteers

Cigarette smoking induces a significant oxidant effect related to variety of free radical-related diseases often affecting the upper respiratory tract, unless it is effectively compensated by the antioxidant barriers of the humans. In the present study, the evaluation of the antioxidant compensatory mechanisms, by estimating the antioxidant capacity of extracellular defence (saliva and plasma) and the intracellular resistance of peripheral lymphocytes to oxidative stress in young healthy smokers, was investigated. Twenty young healthy male smokers and 20 age-matched non-smokers with similar dietary profiles were enrolled in the study. Total saliva and plasma samples were collected from both groups, and total antioxidant capacity (TAC) and lag time were estimated. The latter was also repeated in smokers just after a cigarette smoking. Peripheral lymphocytes isolated from the subjects of both groups were also tested for their inherent DNA damage as well as for their ability to resist H2O2-induced DNA damage by using the comet assay. TAC of plasma was found significantly higher in smokers compared to non-smokers (p <0.004), whereas no difference was recorded in plasma lag time values. Lymphocytes of smokers manifested a significantly decreased oxidant resistance (increased DNA fragmentation) to H2O2, in comparison to non-smokers. Our results indicate that young smokers do not manifest different salivary antioxidant defence than non-smokers. They exhibit, however, a higher plasma antioxidant capacity, but a significantly reduced ability of blood lymphocytes, to resist to H2O2-induced DNA damage.     

Ibuprofen inhibits adhesiveness of monocytes to endothelium and reduces cellular oxidative stress in smokers and non-smokers

BACKGROUND: Cigarette smoking is a major risk factor in atherosclerosis and a useful model from which to study chronic inflammation. We compared monocyte function, lipid profiles and inflammatory markers in smokers and non-smokers, before and after oral ibuprofen intake. The adhesion of freshly isolated monocytes to native and tumour necrosis factor alpha (TNFalpha) stimulated human umbilical vein endothelial cells (HUVEC), as well as superoxide anion (O2-) levels and hydrogen peroxide (H2O2) production in resting and phorbol myristate acetate (PMA) stimulated monocytes were determined. MATERIALS AND METHODS: A group of nine smokers without any other coronary risk factor was compared with an age-matched group of 9 non-smokers. Tests were performed before and after a two-week course of oral ibuprofen (600 mg day-1). RESULTS: In smokers before ibuprofen, monocyte adhesion to native and TNFalpha-stimulated HUVEC was increased (P < 0001 and P < 0.01, respectively), and so were O2- levels in native and PMA-stimulated monocytes (P < 0.01 and P < 0.001, respectively). Ibuprofen reduced the adhesion of monocytes to native and stimulated HUVEC (P < 0.001) and O2- generation by resting and PMA-stimulated cells (P < 0.01) in both groups. H2O2 production by resting and PMA-stimulated monocytes was reduced in smokers and non-smokers (P < 0.01). Interestingly, ibuprofen increased HDL cholesterol levels in smokers (P < 0.01) and non-smokers (P < 0.001), and reduced the level of triglycerides in smokers (P < 0.05). CONCLUSION: Oral administration of ibuprofen reduced the adhesion of monocytes to HUVEC, suppressed oxidative stress and increased HDL cholesterol levels in smokers and non-smokers.     

Serum amyloid A low-density lipoprotein levels and smoking status in obese Japanese patients

Serum amyloid A low-density lipoprotein (SAA-LDL) is formed by an oxidative interaction and is considered to be a new marker related to oxidative modification of LDL. As the effect of smoking on oxidized LDL is of concern, this study investigated the association between SAA-LDL and smoking status. A total of 578 Japanese obese outpatients (mean ± SD age 50.5 ± 14.3 years) were studied. Smoking status was examined via a self-reported questionnaire. Cardio metabolic variables, including high-sensitivity Creactive protein (hsCRP), were analysed in addition to SAA-LDL. There was an increasing trend in SAA-LDL levels from non- to ex- to current smokers, and significantly higher SAA-LDL levels were observed in current smokers versus non-smokers (median SAA-LDL level 36 μg/ml versus 28 μg/ml, respectively). This significant difference was reduced after adjusting for multiple confounders, including lipid levels. Smoking may be associated with increased levels of SAA-LDL in an obese Japanese population, but further studies are needed.     

Acute effect of cigarette smoking on serum angiotensin-converting enzyme activity in normal man

The acute effect of cigarette smoking on serum angiotensin-converting enzyme activity was evaluated in 6 healthy subjects consisting of 4 non-smokers and 2 habitual smokers. Cigarette smoking resulted in rapid increases in serum converting enzyme activity in 5 of 6 subjects within 5 min. and the converting enzyme activity remained above the control value at 30 min. The increase in the enzyme activity of non-smokers was higher than that of habitual smokers at any time when the enzyme activity was determined. It is therefore suggested that cigarette smoke (or smoking) can cause the secretion of angiotensin-converting enzyme from the pulmonary endothelial cell, in which the enzyme may be produced, to the systemic circulation. It is also speculated that the increase in the enzyme activity may contribute to the initiation of cardiovascular changes associated with cigarette smoking.     

The effect of smoking on the urinary excretion of 8-oxodG and 8-oxoGuo in patients with type 2 diabetes

Over the past decades, attention has been paid to understanding the impact of oxidative stress and related modifications of DNA and RNA on various human health risks. A recent meta-analysis comprising 1915 smokers and 3462 non-smokers found a significantly higher level of DNA oxidation measured as urinary 8-oxo-7, 8-dihydro-2′-deoxyguanosine (8-oxodG) excretion in smokers compared with non-smokers in a healthy population. We aimed to investigate if an increased urinary excretion of 8-oxodG in smokers versus never smokers and former smokers could be verified in a population with type 2 diabetes. Additionally, we measured RNA oxidation levels through urinary excretion of 8-oxo-7, 8-dihydroguanosine (8-oxoGuo). Our study included urinary samples from 2721 type 2 diabetic patients, analyzed using ultra-performance liquid chromatography tandem mass spectrometry (UPLC-MS/MS). Logistic regression was used to examine the relationship between daily smokers (n?=?462) versus former (n?=?1341) and never smokers (n?=?918) regarding the RNA and DNA oxidation, respectively. We did not find any significant effect of smoking on urinary excretion of 8-oxodG or 8-oxoGuo in our study. Due to a sparse study area, it is still too early to draw any conclusions on smoking and RNA-oxidation. Regarding DNA oxidation, our study suggests that the effect of smoking seen in healthy populations might be attenuated in patients with type 2 diabetes.     

Levels changes of blood leukocytes and intracellular signalling pathways in COPD patients with respect to smoking attitude

OBJECTIVES: To examine whether the proportions of blood leukocyte subsets are altered in COPD, and to assess the disturbances in signalling pathways in the leukocytes of COPD patients, with respect to smoking history. DESIGN AND METHODS: The study was performed at the Faculty of Pharmacy and Biochemistry and University Hospital for Lung Diseases, Zagreb, Croatia. Leukocyte counts were determined in 28 COPD male patients (11 smokers, 9 ex-smokers, 8 non-smokers) and 42 healthy male subjects (15 smokers, 13 ex-smokers, 14 non-smokers). We assessed activation of MAPKs (ERK, JNK, p38), and expression of Bcl-2 and Bax in the leukocytes by western blotting. RESULTS: Neutrophil and monocyte percentages were significantly increased, and lymphocyte percentage significantly decreased in COPD patients compared with healthy subjects (p<0.05). However, no significant smoking effect regarding leukocyte subsets was observed when compared current or former smokers with non-smokers of each studied group. ERK was activated in non-smokers only, especially in healthy ones. In contrast, strong induction of JNK and p38 phosphorylation, decreased Bcl-2 levels and increased Bax levels were detected in COPD smokers and COPD ex-smokers, but also in healthy individuals who smoke compared with healthy non-smokers (p<0.05). CONCLUSION: These results show that COPD and smoking affect intracellular signalling pathways. Understanding of the basic cellular and molecular mechanisms in COPD is essential for identification of molecules that may serve as targets for diagnosis and therapeutic interventions.     

吸烟对血清高密度脂蛋白胆固醇水平影响的研究

目的探讨吸烟对血清高密度脂蛋白胆固醇(HDL-C)水平的影响程度。方法采用调查问卷与血脂检测相结合的方法,对1741例目前正保持吸烟习惯者与3533例未建立吸烟习惯或已戒烟者的HDL-C水平进行分析;为进一步排除饮酒对HDL-C的影响,还筛选出245例只吸烟不饮酒者,比较不吸烟与吸烟两组HDL-C水平的差异。结果吸烟组的HDL-C水平为1.28mmol/L,不吸烟组的HDL-C水平为1.43mmol/L,两组相比差异具有高度统计学意义(P<0.01);吸烟且不饮酒组的HDL-C水平为1.22mmol/L,与不吸烟组相比差异具有高度统计学意义(P<0.01)。结论吸烟可以导致血清HDL-C水平降低,这或许是吸烟导致冠心病和缺血性脑卒中危险增加的有效机制之一。     

Effects of smoking on regional cerebral blood flow in cerebral vascular disease patients and normal subjects

The chronic effect of smoking on the regional cerebral blood flow (r-CBF) was studied by 133-Xenon inhalation method and described with the Initial Slope Index (ISI). Fifty-two patients as the control group who had no abnormality neurologically or with CT scan, 32 patients with old cerebral infarction and 20 patients with old cerebral hemorrhage were introduced to the present study, and these patients were divided into smokers and non-smokers in each group. Those whose smoking index of 200 or more [(number of cigarettes/day) X (years of smoking history) greater than or equal to 200] were designated as smokers. ISI values were decreased significantly in smokers than non-smokers in all groups. Mean ISI value of unaffected hemisphere in smokers decreased by 16% in the infarction group and 22% in the hemorrhage group comparing to the non-smokers', respectively. In the control group, mean ISI value of right hemisphere decreased by 15% and left 14% in smokers compared to the non-smokers. The r-CBF values in 44 of the 47 smokers were found to be lower than the expected age matched values in non-smokers. Serum high density lipoprotein cholesterol value in smokers was significantly lower than that in non-smokers. We demonstrated preliminarily that the smoking chronically reduced the r-CBF. Advanced atherosclerosis associated with the smoker was suggested to affect the CBF.     

Serum angiotensin converting enzyme activity in cigarette smokers

Low activity of angiotensin converting enzyme (ACE) has been reported in patients with smoking related diseases, such as chronic bronchitis, emphysaema and carcinoma of the lung [1] but this has not been reported in healthy, chronic smokers. Serum ACE was measured in 40 healthy cigarette smokers and in 42 healthy non-smokers. The mean value was significantly lower in the smokers. Hence a non-smokers. The mean value was significantly lower in the smokers. Hence a patient's smoking habits should be taken into consideration when assessing the significance of his serum ACE levels.     

Smoking is associated with a high prevalence of microalbuminuria in hypertensive high-risk patients: data from I-SEARCH

Background

Microalbuminuria (MAU) is a marker of endothelial dysfunction and a predictor of cardiovascular events. The effects of cigarette smoking on the prevalence of MAU in a high-risk population with arterial hypertension are unclear.

Methods

The International Survey Evaluating Microalbuminuria Routinely by Cardiologists in patients with Hypertension (I-SEARCH) documented the clinical profile of 20,364 patients with arterial hypertension and cardiovascular risk factors. In this population, 13,690 patients had no history of smoking, 4,057 patients were former smokers and 2,617 patients were current smokers.

Results

The prevalence of MAU was associated with the smoking status. Consumption of 1–20 cigarettes per day leads to an increase of 6.8% in the prevalence of MAU compared to non-smokers (P < 0.001). Smoking of >20 cigarettes per day was associated with a 12.5% higher prevalence of MAU compared to non-smokers, while former smokers had a 4.7% higher prevalence of MAU. Multivariable analysis revealed that smoking was independently associated with MAU [odds ratio (OR) smoking vs. non-smoking 1.16; 95% confidence interval (CI) 1.01–1.33; P < 0.05]. Particularly, a consumption of >20 cigarettes per day was associated with high odds for MAU (OR 1.33; CI 1.01–1.75; P < 0.05). Interestingly, independently of blood pressure, the use of an angiotensin receptor blocker and an ACE was associated with significantly reduced odds ratio for MAU in the smoking group, while there was no significant association in the non-smoking group.

Conclusion

The prevalence of MAU in hypertensive patients is higher in smokers than in non-smokers with a strong dose dependency.     

Smoking depresses adipose lipoprotein lipase response to oral glucose

Adipose tissue lipoprotein lipase was studied in smokers (n = 17) aged 18-47 years and compared with enzyme activity in non-smokers of comparable age (n = 8) and a second time in some of the subjects 5-9 weeks after cessation of smoking (n = 7). Serum cotinine levels served to validate the smoking status of the subjects. Fasting enzyme activity was similar in smokers and non-smokers, when expressed per 10(6) cells, but was significantly increased when normalized for cell size. When lipoprotein lipase was determined in the same individual 4 h after an oral glucose load, a significant decrease (P less than 0.002) occurred in the smokers, while enzyme activity rose in the nonsmokers (P less than 0.02). A tendency for enzyme activity to rise after oral glucose was seen in ex-smokers, which did not reach statistical significance. Even though the mean serum insulin and glucose levels did not differ in the three groups of subjects, the per cent decrease in lipoprotein lipase after oral glucose in smokers was negatively correlated with insulin release into serum in the same subject, i.e., the greater the insulin release, the less the decrease in lipoprotein lipase activity. We would like to propose that the lower body weight in smokers is related to the paradoxical response of adipose tissue lipoprotein lipase to carbohydrate and that the reversal of this behaviour contributes to the weight gain often observed after cessation of smoking.     

Maintained hyperexcretion of thromboxane A2 metabolite in healthy young cigarette smokers: results from a prospective study in randomly sampled males with stable smoking habits

Summary. Although several studies have identified cigarette smoking as a factor increasing platelet formation of thromboxane A₂ (TxA₂), no prospective data on this issue have been presented in a defined population with stable smoking habits. Therefore, we analysed the relation between smoking habits and urinary excretion of the 2, 3-dinor metabolites of thromboxane A₂ (Tx-M) and prostacyclin (PGI-M) in 87 males, randomly sampled from a population of 18–19-year-old men, at two different occasions separated by 31–49 months. The daily cigarette consumption among the smokers was unchanged between the study occasions (11 vs. 11 cigarettes day^-1), but 9 of 43 initial smokers had quit. None of the initial non-smokers had begun smoking. Tx-M was higher in the smokers than in the non-smokers and correlated with the daily cigarette consumption both at the initial (176 vs. 123 pg mg^-1 creatinine; P = 0.01) and the second (214 vs. 164 pg mg^-1; P = 0.002) study occasion. Those who had quit smoking since the initial study did not differ in Tx-M from the non-smokers at the second study occasion. Urinary PGI-M did not differ between cigarette smokers, non-smokers and quitters at either of the study occasions. We conclude that cigarette smoking elicits an increased formation of thromboxane A₂, indicating platelet activation, that is stable during an observation period of up to 4 years. The increased platelet activity is reversible upon quitting.     

Antipyrine clearance and metabolite formation: the influence of liver volume and smoking

The influence of liver volume and cigarette smoking on antipyrine clearance and metabolite formation was studied in seventeen volunteers (eight smokers, nine non-smokers). Inter-test coefficient of variation of liver volume (as determined by ultrasound) was 6.3%. The mean antipyrine clearance was 49.3 +/- 18.3 ml min-1 and when normalized for liver volume 36.1 +/- 10.1 ml min-1 l-1. The antipyrine clearance per unit volume of liver was significantly higher in smokers (43.0 +/- 10.5 ml min-1 l-1), than in non-smokers (30.0 +/- 4.6 ml min-1 l-1) (P less than 0.01). No significant difference was found between the two groups as to the excreted amounts of 4-hydroxyantipyrine (OHA), norantipyrine (NORA), and 3-hydroxymethylantipyrine (HMA). Normalized for liver volume the mean clearances for production (Clm) of these metabolites were significantly higher in the group of smokers than in the group of non-smokers. The greatest change was observed for OHA formation. However, analysis of variance showed that the differences in the percentages of change of the mean Clm of these metabolites in the two groups are not significant.     

Cigarette smoking and hypertension influence nitric oxide release and plasma levels of adhesion molecules.

Progression of atherosclerosis is currently believed to involve interactions between leukocytes and vascular endothelium. Epidemiological risk factors for atherosclerosis such as hypertension and smoking are known to cause endothelial dysfunction, which is an early event in the atherosclerotic process; they also may be considered in the light of their effects on adhesion molecule expression and release. Little is known about the additive effect between these two risk factors on endothelial adhesion molecule expression and nitric oxide release. Soluble adhesion molecules and the nitric oxide were quantified in smoking hypertensive patients in comparison to those from patients with hypertension alone. Cotinine, a stable metabolite of nicotine, has been used to identify smokers. One hundred and three hypertensive patients were selected: 51 smokers (plasma cotinine levels >25 ng/ml) and 52 non-smokers. Plasma concentrations of soluble intercellular cell adhesion molecule-1 (sICAM-1), soluble endothelial leukocyte adhesion molecule-1 (sELAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-I) were quantified with ELISA methods. Plasma concentration of nitric oxide metabolites was measured by HPLC, whilst plasma concentration of cotinine was measured by RIA. Significant increases of sICAM-1 and sVCAM-1 were demonstrated in smokers (p<0.001 and p<0.05, respectively). In the same patients, a positive significant correlation between sVCAM-1 and plasma cotinine levels was observed (p<0.002). Nitric oxide metabolites were reduced significantly (p<0.04) in smokers. In conclusion, our data show that the two risk factors, smoking and hypertension, are additive risk factors in generating endothelial dysfunction and vascular damage, which plays a key role in atherogenesis.     

Relationship between smoking status and serum lipids in a hyperlipidemic population and analysis of possible confounding factors.

The aim of our study was to estimate the potential relationship between smoking behavior and other coronary heart disease risk factors in 250 hyperlipidemic patients. We present data obtained through self-reporting of the number of cigarettes smoked per day, measurements of three tobacco markers, and data on dietary habits and lipid variables. We measured cotinine (by HPLC) and thiocyanate and used a recent colorimetric assay for the indirect evaluation of the nicotine metabolites in a single urine specimen. Mean values of nicotine metabolites, expressed as cotinine equivalents, were 6.7, 39.9, and 79.4 mumol/L, respectively, for nonsmokers, light smokers (7.7 cigarettes per day), and heavy smokers (25.8 cigarettes per day). We found that light smokers have higher concentrations of cotinine and nicotine metabolites in proportion to the number of cigarettes smoked per day than do heavy smokers. Thus, the simple colorimetric assay can accurately evaluate smoking status. Hyperlipidemia and smoking are linked by an intricate network of multiple relations. The concentration of high-density lipoprotein (HDL) cholesterol is lower in heavy smokers, and the concentrations of triglycerides and cholesterol are higher. The 0.11 mmol/L difference in HDL cholesterol between light and heavy smokers is close to the results of previous papers; however, when gender, dietary habits (including alcohol intake), and data on body mass index are included in a multiple regression analysis, there is no longer an association between HDL cholesterol concentrations and smoking status. Therefore, these different dietary habits may be confounding factors that partly explain the pattern of lipid variables.     

Long-term cigarette smoking increases the prevalence of carotid artery calcification seen on panoramic dental radiographs in male patients

Panoramic dental radiographs are commonly used in general dentistry and oral and maxillofacial surgery to examine upper and lower teeth, maxilla, mandible and the surroundings simultaneously. Carotid artery calcification, a specific indicator of atherosclerotic change of the carotid arteries, can be seen on the radiographs. Many studies have suggested that cigarette smoking is a risk factor of atherosclerotic change as well as cerebral infarction. We hypothesized that smoking could increase the prevalence of carotid artery calcification, and compared the radiographs of smokers and non-smokers aged 50 years and over: 146 male smokers, 165 male non-smokers, 42 female smokers and 422 female non-smokers. This is the first study to focus on carotid artery calcification seen on panoramic dental radiographs to show the connection between smoking and atherosclerotic change. In male patients, carotid artery calcification was seen in 18 (14.1%) of the smokers, and in 8 (4.8%) of the non-smokers, which clearly shows that male patients aged 50 years old or over are more likely to develop carotid artery calcification if they smoke. However, there is no significant difference between female smokers and female non-smokers in the same age group. Dentists are in a good position to find carotid artery calcification on radiographs. When this is found on a radiograph, the patient should be advised to stop smoking and be referred to a physician for further tests. Clinicians should be aware that this radiographic finding indicates the presence of atherosclerotic change of the carotid arteries.     

Do nurses smoke because of stress?

A comparison of learner nurses and student teachers indicated that occupational differences in smoking prevalence were established prior to entry. However, learner nurses experienced higher stress for the greater part of their first year of training and this was one factor contributing to the consolidation of smoking among them. In general, smoking was seen as a way of dealing with negative feelings and although smokers did not experience greater stress than non-smokers, the former were more likely to feel anger. Lower levels of perceived stress were associated with moves to lesser smoking, suggesting that stress prevents smoking being given up. Some non-smokers were vulnerable in that they both experienced higher stress and saw smoking as a solution. The use of maladaptive intrapsychic coping techniques and the absence of social support outside nursing were both associated with movements to greater smoking.     

Monitoring micronutrients in cigarette smokers

Smoking is associated with oxidative stress and increased risks of many chronic diseases that both shorten life and impair its quality. Low concentrations of several micronutrients, especially the antioxidants vitamin C and beta-carotene, are also associated with smoking, and there has been much interest in determining whether deficiencies in micronutrients are involved etiologically in smoking-related diseases. The objective of this review was to bring together reports on dietary intakes, biochemical indicators of micronutrient status, and results of some intervention studies on micronutrients where authors had compared outcomes in smokers and non-smokers. The micronutrients discussed are vitamins A, E, and C; the carotenoids; some of the B-vitamin group; and the minerals selenium, zinc, copper, and iron. The data were then examined to determine whether effects on the biochemical markers of micronutrient status were due to differences in dietary intakes between smokers and non-smokers or to the consequences of inflammatory changes caused by the oxidative stress of smoking. It was concluded that although smoking is associated with reduced dietary intake of vitamin C and carotenoid-containing foods, inflammatory changes increase turnover of these micronutrients so that blood concentrations are still lower in smokers than non-smokers even when there is control for dietary differences. In the case of vitamin E, there is some evidence for increased turnover of this nutrient in smokers, but this has little to no influence on blood concentrations, and there are no differences in dietary intake of vitamin E between smokers and non-smokers. Serum concentrations of vitamin A, folate, and vitamin B12 and B6 markers do not appear to be influenced by smoking, although there is some influence of dietary intake on concentrations of these nutrients in the body. In the case of the minerals examined, the main effects on biochemical markers of mineral status were attributed to inflammation and were therefore greater in heavy or long-term smokers. Serum concentrations of selenium and erythrocyte GPx activity were lower in smokers. Erythrocyte CuZn-SOD activity and serum ceruloplasmin concentrations were elevated, while serum zinc concentrations were depressed only in heavy smokers. Lastly, smoking appears to affect iron homeostasis mainly by changing hemoglobin concentrations, which were in general increased. Serum iron, TfR, and ferritin were mostly unaffected by smoking, except in pregnancy where there is evidence of increased erythropoiesis causing lower saturation of plasma transferrin and some evidence of lowering of iron stores.