Cigarette smoking causes accumulation of polymorphonuclear leukocytes in alveolar septum

The polymorphonuclear leukocyte (PMN) may play an important role in the pathogenesis of emphysema. Cigarette smoking is associated with the accumulation of PMN in the lung as determined by bronchoalveolar lavage. We enumerated alveolar wall PMN on histologic sections from lungs of humans and hamsters with and without cigarette smoke exposure. In human nonsmokers, there were 0.9 +/- 0.2 PMN/mm alveolar wall. In cigarette smokers without emphysema, there were 2.1 +/- 0.3 PMN/mm alveolar wall (p less than 0.01), and in cigarette smokers with emphysema, there were 2.4 +/- 0.7 PMN/alveolar wall (p less than 0.05). There were 1.7 +/- 0.3 PMN/mm alveolar wall in the lungs of hamsters unexposed to cigarette smoke compared with 3.1 +/- 0.3 PMN/mm alveolar wall in smoke-exposed hamsters (p less than 0.005). Although cigarette smoking causes PMN to accumulate within alveolar septa, the accumulation does not seem to be closely related to the development of emphysema. This suggests that additional or other factors are important in the pathogenesis of emphysema.     

Lung phagocyte recruitment and metabolic alterations induced by cigarette smoke in humans and in hamsters

Cigarette smokers had an increased number of alveolar macrophages (AM) that had temporally related increases in oxidative metabolism in vitro compared with that in nonsmokers. The AM from young asymptomatic human cigarette smokers had a selective increase in superoxide anion (O2) release compared with those from nonsmokers. The AM from older smokers had a more intense, generalized enhancement of oxidative metabolism. Smoking hamsters had similar patterns of lung phagocyte recruitment and increased macrophage oxidative metabolism. The accumulation of AM within the alveolar ducts in smoking hamsters was strikingly similar to that seen in human smokers. The temporal patterns of smoke-induced changes in oxidative metabolism by AM from hamsters and humans were the same. Filtration of particulate constituents from cigarette smoke completely abrogated the distal airway inflammation and the metabolic alterations observed in smoking hamsters.     

Antioxidant enzymatic activities in human blood cells after an allergic reaction to pollen or house dust mite.

Several diseases have been related to oxidative stress. Recently, antioxidant functions have also been linked to anti-inflammatory properties. Cell defenses against reactive oxygen species include antioxidant enzymes. We studied the enzymatic antioxidant capacity in human blood of both red blood and mononuclear cells from patients suffering from an allergic reaction to pollen or house dust mite. We determined superoxide dismutases (SODs), glutathione peroxidase (GSHPx) and catalase (CAT) activities in each cell type. We also determined the extent of thiobarbituric acid reactive substances (TBARS), in order to study the correlation between the cellular enzymatic activities, the redox status and the disease. In mononuclear cells from allergic patients, SODs and CAT activities were enhanced compared to controls. Conversely, a decrease in GSHPx activity was found. In erythrocytes, higher values for GSHPx and SODs and similar CAT activities were found in allergic patients and controls. Interestingly, CuZnSOD and MnSOD activities were enhanced in the same proportion for both, erythrocytes and mononuclear cells. TBARS were also enhanced in both types of cells. The respective enzymatic imbalances in mononuclear cells and erythrocytes, namely, GSHPx/SOD and CAT/SOD, and their consequences are discussed. To our knowledge, this is the first global study of antioxidant enzymes, including TBARS level determinations, in allergy.     

Comparison of the antioxidant enzyme levels with the degree of dysfunction in patients with myocardial dysfunction]

OBJECTIVE: Myocardial dysfunction in patients with cardiomyopathy is proposed to occur due to membrane changes caused by oxidative stress. In our study we evaluate whether there is any relation between the degree of myocardial dysfunction and antioxidant enzymes. METHODS: We studied superoxide dismutase (SOD), glutathione peroxidase (GSHPx) and catalase (CAT) enzyme activities from blood samples of 60 patients (30 patients had ejection fraction (EF) < %35 and 30 patients had EF= %35-50) who have myocardial dysfunction according to clinical findings and two-dimensional echocardiography, and 20 healthy volunteers. RESULTS: We found erythrocyte SOD enzyme activities of patients with EF < %35 (group 3) were significantly lower than in control subjects (group 1) (p=0.01). However in group 2 patients (EF= %35-50), erythrocyte SOD activities were found to be lower than in control subjects but this difference was not significant. Erythrocyte CAT and GSHPx enzyme activities of group 3 were also significantly lower than in control group (p=0.04 and p=0.02 respectively). CONCLUSION: In conclusion, reactive oxygen species play a significant role in the initiation and the progression of congestive heart failure. Increased free radicals levels may cause myocardial muscle dysfunction.     

Possible involvement of free radicals and antioxidants in the early stages of the development of cardiomyopathy in BIO 14.6 Syrian Hamster.

The BIO 14.6 cardiomyopathic Syrian hamster is a well-known animal model of congestive cardiomyopathy. To evaluate the role of free radicals and antioxidant protection in the pathogenesis of cardiomyopathy in this animal, we studied the concentration of heart mitochondrial free radicals, the activities of glutathione peroxidase (GSHPx) and superoxide dismutase (SOD), and the effect of alpha-tocopherol on the early stage of myocardial damage (up to 90 days). The GSHPx activity in BIO 14.6 hamsters was found to be twice that in the normal control hamsters at 30 days of age, while SOD activity was unchanged at 30 and 90 days of age. The concentrations of mitochondrial free radicals in BIO 14.6 hamsters at 40 and 90 days of age were significantly higher than those in the normal control hamsters. A protective effect of alpha-tocopherol therapy was shown in BIO 14.6 hamsters treated during the early stage of cardiomyopathy (up to 90 days). These results show the role of free radicals and antioxidant protection in the pathogenesis of hamster cardiomyopathy. We suspect that an increase in the GSHPx activity in BIO 14.6 hamsters may be due to a compensatory mechanism to counteract oxidative stress, but antioxidant reserve was not sufficient to protect the heart from the toxic effects of increased free radicals in the early stage of cardiomyopathy.     

Cathepsin D activity is increased in alveolar macrophages and bronchoalveolar lavage fluid of smokers

Cathepsin D activity was determined in alveolar macrophages (AM) and cell-free bronchoalveolar lavage fluid (BALF) from volunteers who were current cigarette smokers and compared with that found in lifetime nonsmokers. Enzyme activity was determined with a highly sensitive and specific substrate [D-Phe-Ser(0-CH2-C6H5)-Phe-Phe-Ala-Ala-pAB]. Specific activity was more than three times higher in AM from smokers than in cells from nonsmokers (37,880 +/- 2,090 versus 10,300 +/- 1,200; p less than 0.001) and approximately seven times higher in BALF from smokers than from nonsmokers (3,620 +/- 490 versus 515 +/- 165; p less than 0.001). This study demonstrated that cigarette smoke is a potent inducer of cathepsin D activity in AM in vivo. Because cathepsin D is capable of degrading a variety of proteins, the finding of high concentrations of the enzyme in AM and BALF from smokers, along with previous observations of elevated cathepsin B activity, suggests that lysosomal enzymes may cause or contribute to structural lung damage associated with cigarette smoking.     

Activity of antioxidant enzymes and concentrations of thiobarbituric acid reactive substances (TBARS) in melanotic and amelanotic Bomirski melanoma tissues in the golden hamster (Mesocricetus auratus,Waterhouse)

The activity of superoxide dismutase (SOD) and glutathione peroxidase (GSHPx), as well as the concentration of thiobarbituric acid reactive substances (TBARS) in tissues of transplantable melanoma in the golden hamster were measured and compared. Ten inbred male hamsters were used for the experiment. They were divided into two groups and were given Bomirski melanoma cells subcutaneously. The first group was given melanotic (Ma) melanoma cells. The second group was given amelanotic (Ab) melanoma cells. Thirty days after the transplantation the hamsters were dissected and the tumor tissues were taken and homogenized. A statistically significantly higher activity of the measured antioxidant enzymes was found in homogenates of Ma tumor than in homogenates of the Ab tumor. Activity of SOD is 8% higher in melanotic melanoma, 24% higher in CAT, and 45% higher in GSHPx. Statistically significant differences between TBARS concentrations were not confirmed. The higher activity of antioxidant enzymes in the melanotic tumor is a result of increased generation of oxygen-derived free radicals. It is presumed that it is strictly connected with intensified production of quinone and semiquinone radicals in the process of melanogenesis.     

Altered oxidative metabolic responses in vitro of alveolar macrophages from asymptomatic cigarette smokers

Superoxide anion (O2) release by alveolar macrophages (AM) from young asymptomatic cigarette smokers was greater than that by AM from age-matched nonsmokers. Greater O2 release by AM from cigarette smokers was observed before and after stimulation by bacteria or phorbol myristate acetate (PMA). In contrast, oxygen uptake and glucose (1(-14)C) oxidation by unstimulated or stimulated AM from cigarette smokers was the same as that by AM from non-smokers. The selective increase of O2 release by AM from cigarette smokers was not due to a lack of O2 scavenging agent within the cells, since intracellular superoxide dismutase (SOD) was increased in AM from smokers. The potential importance of enhanced O2 release by AM from cigarette smokers was confirmed by demonstrating that lysis of fibroblasts induced by AM from smokers was completely prevented by addition of SOD and catalase.     

Effect of haemodialysis on the oxidative stress and antioxidants in diabetes mellitus

Abstract Oxidative stress has been defined as a loss of counterbalance between free radical or reactive oxygen species (ROS) production and antioxidant systems. It is involved in the pathogenesis of different chronic diseases. High levels of ROS production via different biochemical mechanisms accompany diseases like type 2 diabetes mellitus (DM) and end-stage renal disease (ESRD). Elevated oxidative status and reduced antioxidant defence systems in patients with DM and ESRD accelerate the prevalence of atherosclerosis and other chronic complications. Our aim was to reveal the effects of diabetes and haemodialysis (HD) separately and together on oxidative stress. In our study, we included 20 diabetic (DM) patients with no renal disease, 20 non-diabetic haemodialysis (HD), 20 diabetic haemodialysis (DHD) patients and 20 healthy volunteers. We have determined the levels of lipid peroxidation expressed as thiobarbituric acid-reactive substances (TBARS), oxidative protein damage as indicated by protein carbonyl (PCO) content and activities of antioxidant enzymes including superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSHPx) in all patient groups and healthy subjects. We found enhanced oxidative stress in all patient groups due to an increase in lipid peroxidation (TBARS) and increased oxidative protein damage in terms of PCO content and reduced activities of SOD, CAT and GSH-Px. Oxidative stress was more profound in diabetic patients undergoing haemodialysis. We conclude that both diabetes and dialysis increase oxidative stress and their combined effect on oxidative stress is the highest in magnitude as observed in diabetic patients undergoing haemodialysis.     

The effects of physical exercise on the cigarette smoke-induced pulmonary oxidative response

Studies have shown that the oxidative power of cigarettes is related to the pathogenesis of several pulmonary diseases and that regular physical exercise contributes significantly to reducing the deleterious effects of cigarettes. The objective of the present study was to investigate the therapeutic effects of physical exercise on histological and oxidative stress markers in animals exposed to cigarette smoke. Thirty-six male, eight-week-old C57BL-6 mice were divided into four groups (n = 9 for each group): control, exercise, cigarette smoke, and cigarette smoke plus exercise. The cigarette smoke (CS) groups were exposed to cigarette smoke 3 times/day (4 cigarettes/session) for 60 consecutive days. The exercise groups were submitted to swimming physical training 5 days/week for eight weeks. Forty-eight hours after the last exercise and cigarette exposure, the animals were sacrificed using cervical traction. The right lung was removed, processed, and stored for future analysis. In addition to the analysis of collagen content (hydroxyproline), oxidant production (anion superoxide), antioxidant enzyme activity (SOD and CAT), and lipid and protein oxidative damage (TBARS and Carbonylation), histological and morphological studies were performed. The results revealed that the animals exposed to cigarette smoke showed enlargement and destruction of the alveolar septum and increases in the numbers of macrophages and neutrophils, as well as in the amount of collagen. Our results also showed a decrease in the volume density of elastic fibers and an increase in the volume density of airspaces. However, physical exercise partially improved these markers. Additionally, physical exercise decreased oxidant production and increased the activity of the enzymatic antioxidant defense system, but did not reverse lipid and protein oxidative damage induced by cigarette smoke. These results suggest that physical training partially improves histological and oxidative stress parameters in the lungs of animals chronically exposed to cigarette smoke and that other therapies can contribute to potentiate these effects.     

Antioxidant diet protects against emphysema, but increases mortality in cigarette smoke-exposed mice

Oxidative stress plays an important role in cigarette smoke-induced lung inflammation and emphysema. We produced an enriched diet by adding freeze-dried fruits and vegetables and additional supplements to the 8604 Teklad Rodent Diet, a standard rodent diet. In this study, we examined the effects of the antioxidant-enriched diet on cigarette smoke-induced lung inflammation and emphysema. CH3/HeN mice were fed either a regular diet or the supplemented diet. These mice were exposed to filtered air, a low concentration of cigarette smoke (total particulate matter: 100 mg/m3) or a high concentration of cigarette smoke (total particulate matter: 250 mg/m3) for 6 h/day, 5 days/week for total 16 weeks. Surprisingly, increased mortality (53%) was observed in the high concentration of cigarette smoke-exposed mice fed the antioxidant diet compared to the high concentration of cigarette smoke-exposed mice that were fed a regular diet (13%). The necropsy analysis revealed nasal passage obstruction due to mucous plugging in cigarette smoke-exposed mice on the antioxidant diet. However, the antioxidant diet significantly reduced neutrophilic inflammation and emphysema in the high concentration of cigarette smoke-exposed mice as compared to the regular diet /high concentration of cigarette smoke controls. The antioxidant capacity in the bronchoalveolar fluid or oxidative damage to the lung tissue was not affected by the antioxidant diet. Pro-MMP-2, MMP-2, and MMP-9 activity did not correlate with the protective effects of AOD on cigarette smoke-induced emphysema. These data suggest that the antioxidant diet reduced cigarette smoke-induced inflammation and emphysema, but increased mortality in the obligate nose-breathing mice.     

The Importance of Ultramicroscopic Emphysema in Cigarette Smoke-Induced Lung Disease

To determine the role of the alveolar pores in cigarette smoke-induced lung disease, we examined the alveolar pores of guinea pigs exposed to cigarette smoke for 12 months, and compared these data to those obtained from sham-smoked animals, correlating the data with airspace size and lung function. We found that the smoke-exposed animals had a larger mean number of pores per alveolus (p < 0.001), and the distributions of pore size and shape were significantly shifted to indicate a larger and more irregular pore configuration (p < 0.001, 01 respectively). In the smoke exposed group, there was a significant correlation of pore number with total lung capacity (TLC) (0.68 p < 0.05), RV (0.70, p < 0.05), and FEV(0.1)/FVC(-0.77, p < 0.02). No correlations were identified between pore size or shape and the lung function tests. We conclude that cigarette smoke exposure produces an increase in the number of alveolar pores, a process which we believe represents ultramicroscopic emphysema. These alterations appear to precede any increase in airspace size, and may help to explain abnormal lung function in cigarette smokers without macroscopic emphysema or small airway disease. This is the first study to clearly document an increased number of alveolar pores, with a significant number of either/or large and irregular pores, after chronic smoke exposure, but in the absence of gross emphysema.     

Mirtazapine, a mixed-profile serotonin agonist/antagonist, suppresses sleep apnea in the rat

Reactive oxygen species (ROS) are mediators of chronic tissue damage and fibrosis. Endogenous antioxidants may increase in response to oxidants and reduce tissue injury. We investigated the antioxidant response of the lungs to the chronic release of ROS, as occurs in the immune-specific granulomatous inflammation of chronic beryllium disease (CBD), and compared it with that in healthy controls and individuals exposed to cigarette smoke. The antioxidants superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), and glutathione (GSH) were quantitated in lung epithelial lining fluid (ELF) and serum from control subjects (n = 10), cigarette smokers (n = 8), and individuals with CBD (n = 9). GPx activity and extracellular GPx (eGPx) protein were increased in the ELF of subjects with CBD in comparison with that of control subjects and smokers (eGPx in ELF: controls, 1.3 +/- 0.2 microgram/ml, smokers, 1.9 +/- 0.3 microgram/ml, CBD, 3.8 +/- 0.8 microgram/ml; p = 0.002; GPx U/ml ELF, controls 1.4 +/- 0.3, smokers 1.8 +/- 0.4, CBD, 4.5 +/- 1, p = 0.02). Smokers' ELF had higher levels of GSH than that of controls, but CBD patients' ELF contained much more GSH than that of either controls or smokers (p < 0.001). Increases in GSH were correlated with eGPx, indicating similar inducing mechanisms for these antioxidants. Thus, coordinate augmentation of the glutathione antioxidant system occurs in granulomatous lung inflammation.     

Antioxidant Diet Protects Against Emphysema,but Increases Mortality in Cigarette Smoke-Exposed Mice

Oxidative stress plays an important role in cigarette smoke-induced lung inflammation and emphysema. We produced an enriched diet by adding freeze-dried fruits and vegetables and additional supplements to the 8604 Teklad Rodent Diet, a standard rodent diet. In this study, we examined the effects of the antioxidant-enriched diet on cigarette smoke-induced lung inflammation and emphysema. CH3/HeN mice were fed either a regular diet or the supplemented diet. These mice were exposed to filtered air, a low concentration of cigarette smoke (total particulate matter: 100 mg/m³) or a high concentration of cigarette smoke (total particulate matter: 250 mg/m³) for 6 h/day, 5 days/week for total 16 weeks. Surprisingly, increased mortality (53%) was observed in the high concentration of cigarette smoke-exposed mice fed the antioxidant diet compared to the high concentration of cigarette smoke-exposed mice that were fed a regular diet (13%). The necropsy analysis revealed nasal passage obstruction due to mucous plugging in cigarette smoke-exposed mice on the antioxidant diet. However, the antioxidant diet significantly reduced neutrophilic inflammation and emphysema in the high concentration of cigarette smoke-exposed mice as compared to the regular diet /high concentration of cigarette smoke controls. The antioxidant capacity in the bronchoalveolar fluid or oxidative damage to the lung tissue was not affected by the antioxidant diet. Pro-MMP-2, MMP-2, and MMP-9 activity did not correlate with the protective effects of AOD on cigarette smoke-induced emphysema. These data suggest that the antioxidant diet reduced cigarette smoke-induced inflammation and emphysema, but increased mortality in the obligate nose-breathing mice.     

Effects of melatonin on the oxidant/antioxidant status and lung histopathology in rabbits exposed to cigarette smoke

OBJECTIVES AND BACKGROUND: To evaluate the effects of cigarette smoking on the histopathology and the oxidant/antioxidant status of the lungs and to test the potential antioxidant benefits of melatonin on these induced changes. METHODOLOGY: Rabbits were exposed to cigarette smoke in a glass chamber for 1 h daily for 1 month with or without intraperitoneal melatonin injection. A melatonin control group was given intraperitoneal melatonin only. A control group was exposed to clean air only. At the end of 1 month, animals were sacrificed and lung tissues were examined histopathologically. Blood levels of protein sulphydryls, carbonyls, prostaglandin F2alpha (PGF2alpha), malondialdehyde (MDA), glutathione peroxidase and superoxide dismutase (SOD) were measured. RESULTS: Intraparenchymal vascular congestion and thrombosis, intraparenchymal haemorrhage, respiratory epithelial proliferation, number of macrophages in the alveolar and bronchial lumen, alveolar destruction, emphysematous changes and bronchoalveolar haemorrhage scores were significantly increased in rabbits exposed to cigarette smoke compared with the control group. Protein sulphydryls and SOD levels were significantly decreased; carbonyls, PGF2alpha and MDA levels were significantly increased in the smoke exposed rabbits. Administration of melatonin to rabbits exposed to cigarette smoke caused a reduction in the bronchoalveolar haemorrhage score and blood carbonyls levels. Other parameters were unaffected by melatonin. CONCLUSION: Exposure to cigarette smoke causes severe histopathological changes and negatively affects the oxidant/antioxidant status in the lungs of rabbits. A low daily dose of melatonin has some protective effects on histopathological changes and oxidant/antioxidant status of the lungs in smoke exposed rabbits.     

The antioxidative defense in asthma.

Asthma is a disease characterized by chronic airway inflammation. Generation of oxygen free radicals by activated inflammatory cells produces many of the pathophysiologic changes associated with asthma and may contribute to its pathogenesis. However, the activities of antioxidant enzymes and their relation with asthma have not been well defined. This study was performed to examine the activities of major intracellular antioxidants in mild asthmatic patients. Twelve asymptomatic mild asthmatic patients who never used any antiasthma medication and 13 age- and sex-matched healthy control subjects were selected. The activities of erythrocyte antioxidant enzymes, superoxide dismutase (SOD), catalase (CAT), and glutathione-peroxidase (GSH-Px) were measured spectrophotometrically. The mean SOD activity of asthmatic patients was found to be significantly lower than that of the controls (p < 0.05). There was no significant difference in CAT and GSH-Px activities between patients and controls (p > 0.05). Although the mechanisms underlying the association between asthma and antioxidant system are unclear, according to our findings, decreased antioxidant protection may contribute to the pathogenesis of mild asthma.     

Effects of probucol on changes of antioxidant enzymes in adriamycin-induced cardiomyopathy in rats

OBJECTIVE: The clinical usefulness of doxorubicin (adriamycin, ADR) is restricted by the risk of developing congestive heart failure. Probucol has been reported to completely prevent ADR cardiomyopathy without interfering with its antitumor effects. The current study investigated the effects of ADR and probucol on antioxidant enzyme gene expression during adriamycin-induced cardiomyopathy in a rat model. METHODS: The mRNA abundance by Northern and immunoreactive protein levels by Western blotting of myocardial antioxidant enzymes, glutathione peroxidase (GSHPx), manganese superoxide dismutase (MnSOD) and catalase (CAT) were examined in relation to the enzyme activities in hemodynamically assessed control and treated animals. RESULTS: At 3 weeks post-treatment duration, ADR caused heart failure which was prevented by probucol. MnSOD mRNA abundance as well as protein levels were depressed by ADR treatment by 45% and 20%, respectively, and this change was prevented by probucol. However, the mRNA and protein levels of GSHPx and CAT were not significantly changed by ADR or probucol. ADR had no effect on SOD activity but this enzyme activity was increased by probucol and probucol plus ADR. GSHPx enzyme activity was decreased and oxidative stress as indicated by TBARS was increased by ADR and these changes were also modulated by probucol. CONCLUSION: An increase in oxidative stress, GSHPx inactivation and MnSOD downregulation during ADR cardiomyopathy were prevented by probucol treatment.     

Acute effects of smoke exposure on the cellular and cytokine profile in isolated perfused lungs

The aim of this study was to assess the acute effects of cigarette smoke exposure on cellular and cytokine profile in BAL fluids in an isolated perfused rabbit assay. The experimental animals were categorized into four groups: (1) unexposed controls and (2) cigarette smoke-exposed animals perfused with autologous whole blood; (3) unexposed controls and cigarette smoke-exposed; (4) cigarette smoke-exposed animals perfused with Krebs' Ringer solution containing 5% bovine serum albumin and glucose. Cigarette smoke induced an increase in total cell numbers (mainly alveolar macrophages in BAL fluids) and an increase in the permeability index of BAL. Levels of interleukin 8 were also significantly decreased in BAL fluids due to acute effects of cigarette smoke exposure. The most likely explanation for cigarette smoke-induced increase of inflammatory cells in BAL in lungs is because of the release of pre-existing cells from reservoirs within the lungs. The acute effects of cigarette smoke-induced increase of pulmonary epithelial permeability may also play an important role in the cellular recruitment into airspaces from the lung reservoirs.     

Erythrocyte antioxidant enzymes and blood pressure in relation to overweight and obese Thai in Bangkok

The specific activities of antioxidant enzymes, [eg superoxide dismutases (SOD), glutathione peroxidase (GPX) and catalase (CAT)], anthropometric measurements, including waist/hip ratio of 48 male and 167 female overweight persons (body mass index (BMI) > or = 25.0 kg/m2) compared with a 26 male and 80 female control group (BMI = 18.5-24.9 kg/m2) of Thai volunteers who attended the Out-patient Department, General Practice Section, Rajvithi Hospital, Bangkok, for a physical check-up during March-October, 1998, were investigated. There was a slightly significant difference between the median age of the sexes. The medians of height, weight, and waist/hip ratio in males were significantly higher than those in female overweight and obese subjects. The median of arm circumference (AC), mid arm muscle circumference (MAMC) in males was significantly higher than those in female overweight and obese subjects (p < 0.05). The prevalences of hypertension based on systolic and diastolic blood pressure of > or = 160/> or = 95 mmHg, were 8.3% and 37.5% for males and 5.4% and 18.6% for females, respectively. There was no significant difference between the median of antioxidant enzymes (SOD, GPX and CAT) between the sexes. No significant differences in the antioxidant enzymes in male overweight/obese persons and normal controls were presented, whereas antioxidant enzymes in female overweight/obese persons were statistically lower than in control females (p < 0.05). A significantly higher SOD, GPX, and CAT status was observed in normal subjects compared with overweight/obese subjects (p < 0.01). A higher prevalence of SOD < or = 2,866 U/gHb, GPX (< or = 15.96 U/gHb in females was found, compared with males. A high percentage of lower catalase (CAT < or = 19.2x10(4) IU/gHb) was found in both sexes (64.5% in males and 64.5% in females). In obese subjects (BMI > or = 30.0 kg/m2), there were significantly positive relationships between systolic and diastolic blood pressure, systolic blood pressure and waist/hip ratio, and SOD could be related to weight, BMI as well as GPX and CAT, whereas the opposite result was observed for age and SOD.     

Inhibition of neutrophil adherence and movement by acute cigarette smoke exposure.

Peripheral blood neutrophils were harvested and exposed acutely in vitro to physiologically attainable levels of cigarette smoke. The adherence of radiolabeled neutrophils subsequently to alveolar epithelial cell monolayers was measured. In contrast to control cells, smoke-exposed neutrophils were significantly less adherent and failed to increase their adherence following stimulation with phorbol ester or f-met-leu-phe (fMLP). Flow cytometric analysis of the cell surface adhesion protein CD18 demonstrated no significant change in expression following in vitro smoke exposure and, furthermore, no increase in surface CD18 of smoke-exposed cells following consecutive fMLP stimulation was demonstrated. Acute in vivo cigarette smoking of up to 4 cigarettes also did not alter peripheral blood neutrophil CD18 expression. Cell spreading and chemokinesis, but not chemotaxis, was also impaired following in vitro smoke exposure. These data suggest that acute cigarette smoke may impair the crucial neutrophil functions of adherence and movement. However, the chronic effects of cigarette smoke exposure may clearly differ.