Facilitated nitration and oxidation of LDL in cigarette smokers

BACKGROUND: Cigarette smoking increases the risk of developing atherosclerosis and ischaemic heart disease. Smoking-induced oxidative stress is considered to favour oxidation of low-density lipoprotein (LDL) and subsequently promotes the atherogenic process. We investigated whether peroxynitrite, a reaction product of cigarette smoke, is involved in facilitated oxidation of LDL in smokers. MATERIALS AND METHODS: Plasma LDL was obtained from 10 healthy asymptomatic cigarette smokers and 10 healthy nonsmokers. The state of enhanced oxidative stress in the plasma was assessed by LDL subfraction assay using anion-exchange high-performance liquid chromatography (AE-HPLC) and measurements of thiobarbituric acid-reactive substances (TBARS), 8-hydroxydeoxyguanosine (8-OHdG), vitamin E, 3-nitrotyrosine and 3-chlorotyrosine. RESULTS: Smokers showed a significantly higher level of TBARS and 8-OHdG as well as a significantly lower level of vitamin E than nonsmokers, even after stopping smoking for 10 h or more. The LDL subfraction assay demonstrated an increase in oxidatively modified LDL, as expressed by lower levels of LDL1 and higher levels of LDL2. The 3-nitrotyrosine levels in apolipoprotein B in LDL were significantly higher in smokers than nonsmokers, while the 3-chlorotyrosine levels remained unchanged. In addition, these changes observed in the smokers were further accelerated within 30 min after resumption of cigarette smoking when compared with the levels before smoking resumption. CONCLUSION: The present study suggests that peroxynitrite plays a significant role in oxidative modification of plasma LDL induced by cigarette smoking.     

Smoking and plasma lipoproteins in man: effects on low density lipoprotein cholesterol levels and high density lipoprotein subfraction distribution

Abstract. In a survey of a healthy population (n = 197), LDL cholesterol, plasma triglycerides and VLDL triglycerides were found to be substantially increased and plasma HDL cholesterol decreased in smokers. The lipid-associated atherogenic risk in smokers as assessed by the LDL/HDL ratio was significantly higher [2.89 (SD 1.18, n= 63)] than in non-smokers [2.38 (SD 0.98, n= 86) P < 0.01]. The lower HDL level found in smokers was explained by a lower HDL-2 subfraction as determined by analytical ultracentrifugation. HDL 2b, 2a and 3a, measured by gradient gel electrophoresis, were all lower in the smokers but this was only significant for HDL 2a. Smoking had no effect on Lp(a) levels. HDL cholesterol and HDL-2 were strongly negatively correlated whereas LDL cholesterol and LDL/HDL ratio were strongly positively correlated with the plasma triglyceride concentration. There was a small but significant reduction in plasma CETP activity [non-smokers 49%t/μl (SD 17, n= 90), smokers 43%t/μl (SD 17, n= 66) P < 0.05] but CETP activity was not correlated with any measure of HDL in this population. Smoking was found to be an important independent contributor to the variation in plasma triglyceride, HDL, HDL-2 and LDL/HDL ratio. After correcting for sex, age, BMI, alcohol consumption, oral contraceptive use and plasma triglycerides smoking was still found to be significantly associated with HDL and the LDL/HDL ratio. Upon adjustment for covariant factors the mean differences between smokers and non-smokers for HDL cholesterol, HDL-2 and LDL/HDL were 0.15 mM, 16 mg dl-¹ and 0.39 respectively. There appeared to be important sex differences in the influence of smoking on plasma lipoproteins. In women the main impact of smoking was on triglyceride levels and they in turn affected LDL and HDL. In contrast, in men, smoking had little impact on triglycerides and affected HDL more directly. We conclude that smoking cigarettes has an important effect on plasma lipoprotein metabolism through multiple mechanisms.     

Smoking cessation after stroke: education and its effect on behavior.

Smoking is an independent risk factor for stroke. The purpose of this prospective study was to determine whether significant changes in smoking behavior occurred in a cohort of stroke patients who were educated about risk reduction during their initial recovery period. Participants or their proxies were then contacted at 3 months for a follow-up interview, during which their current location, smoking status, and functional outcome were recorded. Of 405 participants interviewed, 112 were current smokers at the time of stroke. Participants younger than 65 years and Blacks were more likely to be smokers. At 3 months, 48 (43%) of the baseline smokers had quit smoking compared with an estimated rate of 28% previously reported in the literature. The number of participants who smoked > 20 cigarettes per day was 31 at baseline versus 7 at 3 months. This change of behavior was independent of baseline characteristics and the level of poststroke disability. Risk-reduction education provides stroke survivors with the information needed to change their lifestyles. Further research is needed to determine whether this behavior continues beyond 3 months and to determine why some stroke survivors continue to smoke.     

Smoking Status and Pain Level Among Head and Neck Cancer Patients

Smoking is a risk factor for cancer of the upper aerodigestive tract with recidivism rates high even after diagnosis. Nicotine, a major product in tobacco, is a complex drug with multiple characteristics including analalgesic properties. The goal of the study was to examine pain levels in the context of smoking status among patients recently diagnosed with cancer of the upper aerodigestive tract who have not yet received any treatment including radiation, surgery, or chemotherapy. A convenience sample of 112 newly diagnosed head and neck cancer patients (78 men and 34 women) was recruited from clinics at the University of Florida. Smoking rates were: 32% never smoked, 34% former smokers, 34% current smokers. Among current smokers, 62% reported plans to quit in the next 3 months and 38% had tried to quit more than 3 times in the past 5 years. Current smokers reported higher general (sensory and affective) and oral pain levels (spontaneous and functional) and pain-related interference than did never and former smokers (all F's > 8. and P's < .0001) even after controlling for stage of diagnosis. In addition, current smokers reported significantly greater interference from the pain (F_2,73 = 10.5 P < .0001).PerspectiveThis study highlights the importance of understanding self-reported pain in cancer patients who continue to smoke. When pain is elevated, smokers may be motivated to use tobacco as a means of reducing pain, which in turn reinforces smoking behavior. Tobacco cessation programs should include pain management as a component of treatment.     

Smoking Status Among Women in Households With Young Children

purpose . To identify sociodemographic and health-related correlates of smoking status among women in households with young children.
design . A secondary analysis of the 1992 California Behavioral Risk Factor Surveillance System public-use data tape
participants . Women (N = 520) in households with very young children (≤ 5 years of age)
main outcome measures . Current smoking status
results . Approximately 18% were current smokers; more than 40% smoked more than 10 cigarettes each day. A majority of smokers indicated a high level of nicotine addiction, but had plans to quit. Smoking prevalence varied by sociodemographic variables with higher rates for unmarried, less than college educated, and unemployed participants. Health status also was related to smoking, with higher rates among those with poor health and those limited in activities.
conclusions . Smoking is one way of coping with the stressors of daily life, including those associated with caring for young children. Special cessation efforts may be needed for the unemployed, the unmarried woman, and for those in poor health.     

Smoking status, obesity and hypertension in a general population sample: a cross-sectional study

BACKGROUND: In some studies, hypertension is more common in never and former smokers than in current smokers. AIM: To examine the associations between hypertension and smoking status, when divided into subgroups by overweight and obesity. DESIGN: Cross-sectional study. METHODS: We used data from a national health survey with a probability sample of the national population of Germany aged 18 to 79 (n = 6903 with complete data). Smoking status data were collected via questionnaire. Obesity and overweight were assessed by body mass index, hypertension by blood pressure measurement and by participants' statements about antihypertensive treatment. Analyses were adjusted for gender, age, history of coronary artery disease, serum cholesterol levels, alcohol drinking, exercise, and education. RESULTS: Obese former smokers who were abstinent for 3 or more years had an adjusted odds ratio (OR) 3.6 (95% confidence interval, CI 2.3-5.7) for mild hypertension (> or =140 mmHg systolic or > or =90 mmHg diastolic blood pressure) and an adjusted OR 6.5 (95%CI 3.6-11.8) for moderate or severe hypertension (> or =160 mmHg systolic or > or =100 mmHg diastolic). Normal weight never or former smokers did not differ from normal weight current smokers smoking > or =15 cigarettes/day with regard to likelihood of hypertension (normal weight never smokers, OR 1.1, 95%CI 0.8-1.5; normal weight former smokers, abstinent 3 or more years, OR 0.8, 95%CI 0.5-1.3). DISCUSSION: In this nationally representative sample, never or former smoking was unrelated to hypertension among normal weight individuals.     

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   

Prevalence of patients continuing to smoke after vascular interventions

INTRODUCTION: Smoking is one of the most important risk factors for the development and progression of atherosclerosis. Smoking cessation is an obligatory element in the management of vascular problems and in patients scheduled for vascular interventions. The aim of this study was to assess the prevalence of patients smoking before and after vascular surgical procedures and to evaluate the requirements for inpatient programs for smoking cessation and nicotine replacement therapy. METHODS: 500 patients admitted for vascular interventions were included in this prospective study. Smoking status was evaluated both objectively and subjectively. All patients underwent measurements of exhaled breath carbon monoxide to quantify nicotine dependency and all answered a standardized Fagerstr?m questionnaire both on admission and after surgery to identify current smokers. RESULTS: Of 500 vascular patients included in the study, only 70 (14 %) never had smoked, 243 (49 %) had given up smoking before admission and 161 (32 %) were current smokers. Of the current smokers, 64 (40 %) did not smoke during hospitalization but 97 (60 %) continued to smoke in hospital. Of these 97 patients, 78 (80 %) were men and 19 women; their mean age was 61 +/- 4 years (range 40-84). Four patients had surgery for infrarenal aortic aneurysm, 40 underwent carotid endarterectomy and 53 had peripheral arterial occlusive disease (PAD). There was no difference between abstinent patients and continuing smokers in previous cigarette consumption or Fagerstr?m score, a predictor for long-term smoking behavior. Patients with carotid artery stenosis were significantly more abstinent while hospitalized (P = 0.006); patients with PAD, however, were more likely to continue smoking as inpatients (P = 0.004). Sixty-five percent of continuing smokers stated that they would stop smoking in hospital if counseling and nicotine replacement therapy were provided. With regard to their predominant location of atherosclerosis, patients with PAD were less willing than those with carotid stenosis to abstain from smoking while hospitalized (53 % vs 88 %, respectively; P < 0.001). CONCLUSION: A substantial proportion of patients admitted for vascular surgery are smokers. More than half of these continue to smoke in the hospital, an environment where smoking is prohibited by law. Counseling, nicotine replacement therapy and smoking-cessation programs are urgently needed for vascular surgical inpatients.     

The relationship between smoking and quality of life in advanced lung cancer patients: a prospective longitudinal study

Purpose

Smoking is a major cause of lung cancer, and continued smoking may compromise treatment efficacy and quality of life (health-related quality of life (HRQoL)) in patients with advanced lung cancer. Our aims were to determine (i) preference for treatments which promote quality over length of life depending on smoking status, (ii) the relationship between HRQoL and smoking status at diagnosis (T1), after controlling for demographic and clinical variables, and (iii) changes in HRQoL 6 months after diagnosis (T2) depending on smoking status.

Methods

Two hundred ninety-six patients with advanced lung cancer were given questionnaires to assess HRQoL (EORTC QLQ-C30), time-trade-off for life quality versus quantity (QQQ) and smoking history (current, former or never smoker) at diagnosis (T1) and 6 months later (T2). Medical data were extracted from case records.

Results

Questionnaires were returned by 202 (68.2 %) patients at T1 and 114 (53.3 %) at T2. Patients favoured treatments that would enhance quality of life over increased longevity. Those who continued smoking after diagnosis reported worse HRQoL than former smokers or those who never smoked. Smoking status was a significant independent predictor of coughing in T1 (worse in smokers) and cognitive functioning in T2 (better in never smokers).

Conclusions

Smoking by patients with advanced lung cancer is associated with worse symptoms on diagnosis and poorer HRQoL for those who continue smoking. The results have implications to help staff explain the consequences of smoking to patients.

     

Smoking is associated with insulin resistance and cardiovascular autonomic dysfunction in type 2 diabetic patients

BACKGROUND: Smoking and cardiovascular autonomic dysfunction are associated with high mortality in type 2 diabetic patients. This study tested the hypothesis that smoking is associated with insulin resistance/hyperinsulinaemia and cardiovascular autonomic dysfunction in type 2 diabetic patients who are not treated with insulin. MATERIALS AND METHODS: The study patients were 22 current smokers with type 2 diabetes mellitus (age: 57 +/- 5 years, mean +/- SD) and 30 age-matched never-smoked patients with type 2 diabetes mellitus (control group, 57 +/- 8 years). The quality of blood glucose was assessed by fasting plasma glucose (FPG), fasting immunoreactive insulin (F-IRI), homeostasis model assessment (HOMA) index and haemoglobin A1c (HbA1c). The severity of smoking status was expressed by the Brinkman index, which is calculated as number of cigarettes per day multiplied by years of smoking. Cardiovascular autonomic function was assessed by baroreflex sensitivity (BRS), heart-rate variability, plasma norepinephrine concentration and cardiac (123)I-metaiodobenzylguanidine (MIBG) scintigraphic findings. RESULTS: Baroreflex sensitivity was lower in the current smokers group than in the never-smoked group (P < 0.05). Early and delayed (123)I-MIBG myocardial uptake values were lower (P < 0.05, and P < 0.01, respectively) and the percentage washout-rate of (123)I-MIBG was higher (P < 0.0001) in the current smokers group than in the never-smoked group. Fasting immunoreactive insulin (F-IRI) concentration (P < 0.0001) and the homeostasis model assessment (HOMA) index (P < 0.0001) were higher in the current smokers group than the never-smoked group. Multiple logistic regression analysis revealed that smoking was independently predicted by F-IRI and the percentage washout-rate of (123)I-MIBG. CONCLUSIONS: The results of the study suggested that smoking was associated with cardiovascular autonomic dysfunction and hyperinsulinaemia and that F-IRI and the percentage washout-rate of (123)I-MIBG were independent predictors of smoking in these Japanese patients with type 2 diabetes mellitus.     

Increased serum iron may contribute to enhanced oxidation of low-density lipoprotein in smokers in part through changes in lipoxygenase and catalase

BACKGROUND: Increased oxidative stress is considered to be causative for cardiovascular disease (CVD) in smokers, but its mechanisms are still unclear. We compared oxidative stress markers between male smokers and male nonsmokers. METHODS: Twenty-three healthy men (11 nonsmokers and 12 smokers) were enrolled, and blood samples after 12 h of fasting were collected to assess plasma lipids and oxidative stress markers. The effects of iron loading on 12-lipoxygenase (12-LO) expression and activity in human umbilical vein endothelial cells (HUVECs) were tested in vitro to investigate the relevance of iron to oxidation potential in vivo. RESULTS: Higher levels of plasma-oxidized low-density lipoprotein (LDL) and lipid peroxide (LPO), and higher oxidizability of LDL were observed in smokers than in nonsmokers. Higher levels of serum iron and lower levels of plasma vitamin E were observed in smokers than in nonsmokers. Stepwise multiple regression analysis showed that serum iron was an independent determinant for both plasma-oxidized LDL and lag time of LDL oxidation. Iron loading enhanced 12-LO expression threefold and its activity 1.5-fold. Moreover, iron loading decreased catalase expression by 50% and significantly reduced its activity by 75%. CONCLUSIONS: Enhanced oxidative stress in smokers may be due to increased iron levels. Iron-induced modulation of expression and activity of 12-LO and catalase may be relevant to increased iron-related oxidative stress as observed in smokers.     

吸烟和不吸烟急性心肌梗死患者住院期间焦虑、抑郁水平的比较

目的探讨吸烟和不吸烟的急性心肌梗死（AMI）患者在入住心脏监护室（CCU）期间压力水平的差异。方法选择在CCU住院的AMI患者74例,根据患者是否吸烟分为吸烟组（n=33）和不吸烟组（n=41）,采用焦虑自评量表（SAS）和抑郁自评量表（SDS）调查患者的焦虑、抑郁状况。结果74例患者中有焦虑症状的占75．68％,有抑郁症状的占63．51％;吸烟组患者的SAS、SDS评分分别为（64．39±15．39）,（65．80±15．39）分,不吸烟组的SAS、SDS评分分别为（52．50±6．55）,（53．96±5．32）分;吸烟组焦虑、抑郁程度高于不吸烟组,差异均有统计学意义（t=4．15,4．87;P〈0．01）;且吸烟组重度焦虑、抑郁发生率较高。结论吸烟的AMI患者在人住CCU期间表现出更高的焦虑、抑郁水平,护理人员应给予重视,进行有针对性的干预。     

Mentholated cigarette smoking inhibits nicotine metabolism

Smoking mentholated cigarettes has been suggested to convey a greater cancer risk compared with smoking nonmentholated cigarettes. Two of the possible mechanisms by which mentholated cigarette smoking could increase risk are by increasing systemic exposure to tobacco smoke toxins and by affecting the metabolism of nicotine or tobacco smoke carcinogens. To examine these possibilities, we performed a crossover study in 14 healthy smokers, one-half of whom were African-Americans and one-half whites. Subjects were randomly assigned to smoke mentholated or nonmentholated cigarettes for 1 week, then to cross over to the other type of cigarettes for another week. Subjects were confined to a Clinical Research Center for 3 days of each week, during which time blood levels of nicotine and carbon monoxide were measured throughout the day and an intravenous infusion of deuterium-labeled nicotine and cotinine was administered to determine the rate and pathways of nicotine metabolism. The systemic intake of nicotine and carbon monoxide was, on average, not affected by mentholation of cigarettes. Mentholated cigarette smoking did significantly inhibit the metabolism of nicotine (clearance: 1289 versus 1431 ml/min, two sided, p = 0.02). Inhibition of nicotine metabolism occurred both by slower oxidative metabolism to cotinine and by slower glucuronide conjugation. Our data do not support the hypothesis that mentholated cigarette smoking results in a greater absorption of tobacco smoke toxins. Our finding of impaired metabolism of nicotine while mentholated cigarette smoking suggests that mentholated cigarette smoking enhances systemic nicotine exposure.     

Smoking and incidence of diabetes among U.S. adults: findings from the Insulin Resistance Atherosclerosis Study

OBJECTIVE: The objective of this study was to determine the association between smoking and incident diabetes among U.S. adults. RESEARCH DESIGN AND METHODS: The Insulin Resistance Atherosclerosis Study (IRAS) was a prospective study of the associations of insulin sensitivity and cardiovascular risk factors. We examined the relationship between smoking status categories (never, former, and current) and incident 5-year type 2 diabetes among 906 participants free of diabetes at baseline. We also considered the effect of pack-year categories (never, former <20 pack-years, former > or = 20 pack-years, current <20 pack-years, and current > or = 20 pack-years) upon diabetes incidence. RESULTS: Of current smokers, 96 (25%) developed diabetes at 5 years, compared with 60 (14%) never smokers. After multivariable adjustment, current smokers exhibited increased incidence of diabetes compared with never smokers (odds ratio [OR] 2.66, P = 0.001). Similar results were found among current smokers with > or = 20 pack-years with normal glucose tolerance (5.66, P = 0.001). CONCLUSIONS: Smoking shares a robust association with incident diabetes, supporting the current Surgeon General's warnings against cigarette smoking.     

Smoking among Japanese nursing students: nationwide survey

AIM: This paper reports a study estimating the nationwide prevalence of and attitudes towards smoking among Japanese nursing students. BACKGROUND: The World Health Organization established "World No Tobacco Day" in 1987, and has been promoting antismoking measures worldwide since then, with annual themes. It has emphasized that health care professionals, including nurses, as role models for healthy living, should not smoke, and that as promoters of health education they should not seem to justify or condone their patients' smoking. To promote antismoking measures among nurses, it will be necessary to scrutinize the smoking habits and behavior of nursing students and associated factors, and to conduct effective antismoking education and health education before they acquire the smoking habit. METHODS: A cross-sectional survey was carried out through self-administered, closed-ended, structured questionnaires. Questionnaires were mailed to 4169 nursing students at 27 randomly selected vocational nursing schools nationwide. Smoking status, history, and attitudes towards smoking were examined. RESULTS: Smoking prevalence among female nursing students was 23.5%, which was higher than that among the Japanese general female population aged 20-29 (21.9%). Smoker-students were significantly more positive toward smoking than non-smokers in all opinions about health care professionals' smoking. Multiple logistic regression analysis showed that smoking statuses of the people around the participants, dissatisfaction with being a nursing student, and living alone were associated with participants' smoking behaviour. CONCLUSIONS: The results of the present study suggest an urgent necessity to provide effective antismoking measures for nursing students.     

吸烟对脑梗死患者低密度脂蛋白体外氧化延迟时间的影响

目的 探讨吸烟对脑梗死患者血液中低密度脂蛋白(LDL)体外氧化延迟时间的影响.方法 急性脑梗死患者67例,其中37例有吸烟史者作为吸烟组,30例无吸烟史者作为对照组,两组年龄、性别、血压、血脂、血糖及病灶部位、大小和程度差异无统计学意义(均P>0.05).分析测定所有受试者血液中LDL体外氧化延迟时间及空腹静脉血中LDL-总胆固醇、LDL-甘油三酯(TO)、LDL-游离胆固醇水平.结果 吸烟组LDL体外氧化延迟时间明显短于对照组[(77.21±9.1)min和(59.95±8.7)min,P<0.001].吸烟组LDL-总胆固醇、LDL-甘油三酯、LDL-游离胆固醇与对照组比较差异无统计学意义(分别为5.12±0.61与4.63±0.62 mmol/L;0.89±0.07 mmol/L与0.85±0.04 mmol/L;1.71 ±0.43与1.74±0.91 mmol/L,均P>0.05).结论 吸烟可以使脑梗死患者血液中LDL体外氧化延迟时间缩短,减弱LDL的抗氧化能力,加重机体的氧化压力.     

Smoking reduction treatment with 4-mg nicotine gum: a double-blind, randomized, placebo-controlled study

BACKGROUND: Smoking reduction may provide a harm-reduction alternative treatment for smokers who are not ready to quit smoking. This study evaluated the efficacy of nicotine gum in helping smokers reduce or quit smoking. METHODS: This randomized, double-blind, placebo-controlled trial involved 364 smokers who were not ready to quit but were willing to reduce their smoking intensity. Participants received either 4-mg nicotine gum (n = 184) or placebo gum (n = 180) as desired for up to 12 months. The primary outcome was sustained smoking reduction, which was defined as a decrease in daily cigarette consumption of at least 50% compared with baseline. Secondary measures included point-prevalence abstinence, intention to quit, and cardiovascular risk markers. RESULTS: At 4 months, the sustained smoking reduction rate in the nicotine gum group was twice that of the placebo group (15.8% versus 6.7%, P = .008). Point-prevalence abstinence was 6.6% for the nicotine gum group and 2.2% for the placebo group (P = .07). At 13 months, there was a significant difference in the smoking reduction rate for the nicotine (8.2%) and placebo (2.8%) groups (P = .036). At month 13, the abstinence rates were 12% and 4.5% for the nicotine and placebo groups, respectively (P = .012). Concomitant use of nicotine gum and cigarette smoking was well tolerated. Carbon monoxide levels decreased significantly (P = .01). CONCLUSION: Nicotine gum may be an efficacious harm-reduction alternative for smokers who are not ready to quit and may promote smoking cessation, the ultimate goal in the treatment of tobacco dependence.     

Effect of cigarette smoking on the oxidant/antioxidant balance in healthy subjects

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. METHODS: Thirty healthy subjects (15 smokers and 15 nonsmokers) of both sexes were studied. The smokers group had smoked a mean of 14 cigarettes per day for an average of 4.5 years. Fasting serum levels of malondialdehyde (MDA), a marker of oxidative stress, nitric oxide (NO), reduced glutathione (GSH), and vitamin C (ascorbic and dehydroascorbic acids) were measured. RESULTS: Fasting NO concentration was significantly higher in smokers (51.3 +/- 5.3 microM) than in nonsmokers (35.2 +/- 4.8 microM, P < 0.05). The smokers had significantly higher serum dehydroascorbic acid levels (2.4 +/- 0.5 mg/dL, P < 0.03) than the nonsmokers (1.08 +/- 0.08 mg/dL). No significant differences were observed in the levels of ascorbic acid, MDA, and GSH between the smokers and nonsmokers. CONCLUSIONS: Our results suggest that exposure to cigarette smoke increases NO synthesis, such that NO may act in a compensatory way as an inhibitor of lipid peroxidation. Smoking also activates other antioxidative mechanisms such as involving vitamin C. These protective mechanisms appear to be enough in preventing accumulation of oxidative products such as MDA and avoiding oxidative damage.