scholarly journals Olive Phenol Hydroxytyrosol Prevents Passive Smoking–Induced Oxidative Stress

Circulation ◽  
2000 ◽  
Vol 102 (18) ◽  
pp. 2169-2171 ◽  
Author(s):  
Francesco Visioli ◽  
Claudio Galli ◽  
Elena Plasmati ◽  
Serena Viappiani ◽  
Alicia Hernandez ◽  
...  
Author(s):  
Faruk Yıldırım ◽  
Kabil Sermetow ◽  
Ali Aycicek ◽  
Abdurrahim Kocyigit ◽  
Ozcan Erel

2016 ◽  
Vol 42 (5) ◽  
pp. 333-340
Author(s):  
Thiago Brasileiro de Vasconcelos ◽  
Fernanda Yvelize Ramos de Araújo ◽  
João Paulo Melo de Pinho ◽  
Pedro Marcos Gomes Soares ◽  
Vasco Pinheiro Diógenes Bastos

ABSTRACT Objective: To evaluate the effects of passive inhalation of cigarette smoke on the respiratory system of guinea pigs. Methods: Male guinea pigs were divided into two groups: control and passive smoking, the latter being exposed to the smoke of ten cigarettes for 20 min in the morning, afternoon and evening (30 cigarettes/day) for five days. After that period, inflammatory parameters were studied by quantifying mesenteric mast cell degranulation, as well as oxidative stress, in BAL fluid. In addition, we determined MIP, MEP, and mucociliary transport (in vivo), as well as tracheal contractility response (in vitro). Results: In comparison with the control group, the passive smoking group showed a significant increase in mast cell degranulation (19.75 ± 3.77% vs. 42.53 ± 0.42%; p < 0.001) and in the levels of reduced glutathione (293.9 ± 19.21 vs. 723.7 ± 67.43 nM/g of tissue; p < 0.05); as well as a significant reduction in mucociliary clearance (p < 0.05), which caused significant changes in pulmonary function (in MIP and MEP; p < 0.05 for both) and airway hyperreactivity. Conclusions: Passive inhalation of cigarette smoke caused significant increases in mast cell degranulation and oxidative stress. This inflammatory process seems to influence the decrease in mucociliary transport and to cause changes in pulmonary function, leading to tracheal hyperreactivity.


Author(s):  
Lubica Argalasova ◽  
Ingrid Zitnanova ◽  
Diana Vondrova ◽  
Monika Dvorakova ◽  
Lucia Laubertova ◽  
...  

Background: Exposure to ETS (environmental tobacco smoke) is one of the most toxic environmental exposures. Objective: To investigate the association of ETS with physiological, biochemical, and psychological indicators, as well as with urine antioxidant capacity (AC) and oxidative damage to lipids in a pilot sample of healthy pregnant women. Methods: Exposure to ETS was investigated via a validated questionnaire, and urine cotinine and the marker of oxidative damage to lipids via 8-isoprostane concentrations using an ELISA kit. Urine AC was determined by the spectrophotometric Trolox-equivalent antioxidant capacity (TEAC) method. From a sample of pregnant women (n = 319, average age 30.84 ± 5.09 years) in 80, the levels of cotinine and oxidative stress markers were analyzed. Results: Among the 80 pregnant women, 5% (7.4% confirmed by cotinine) reported being current smokers and 25% reported passive smoking in the household (18.8% confirmed by cotinine). The Kappa was 0.78 for smokers and 0.22 for ETS-exposed nonsmokers. Pregnant women in the ETS-exposed group had significantly reduced AC compared to both the nonsmoker (ETS−) and the smoker groups (p < 0.05). Nonsmokers had significantly lower levels of 8-isoprostane than smokers (p < 0.01) and ETS-exposed nonsmokers (p < 0.05). Correlations between urine levels of cotinine and AC were positive in ETS-exposed nonsmokers. Conclusion: A harmful association of active and passive smoking and oxidative stress parameters among pregnant women has been indicated.


2016 ◽  
Vol 59 (1) ◽  
pp. 68-73 ◽  
Author(s):  
Feyza Ustabaş Kahraman ◽  
Emel Torun ◽  
Nurcan Keskin Osmanoğlu ◽  
Suera Oruçlu ◽  
Ömer Faruk Özer

2006 ◽  
Vol 84 (5) ◽  
pp. 523-529 ◽  
Author(s):  
Toru Kato ◽  
Teruo Inoue ◽  
Toshifumi Morooka ◽  
Nobuo Yoshimoto ◽  
Koichi Node

Recent studies have shown that passive smoking impairs vascular endothelial function and induces oxidative stress in humans. However, in most of the previous human data regarding tobacco-induced pathophysiology, vascular endothelial dysfunction and oxidative stress have been separately assessed. This study was designed to determine the association between the acute effect of passive smoking on vascular endothelial function and in-vivo oxidative stress status. We studied 30 healthy male Japanese volunteers (32 ± 7 years) including 15 habitual smokers and 15 nonsmokers. After baseline echocardiographic, hemodynamic recording, and blood sampling, subjects were exposed to passive smoking for 30 min. Endothelium-dependent vasodilation was measured by using % flow-mediated vasodilation (%FMD) of the brachial artery and plasma levels of 8-isoprostane was measured by enzyme immunoassay before and after the passive smoking exposure. Baseline %FMD was lower (4.3% ± 1.2% vs. 10.9% ± 3.1%, p < 0.001) and baseline plasma 8-isoprostane level was higher (41.5 ± 5.8 pg/mL vs. 26.9 ± 5.4 pg/mL, p < 0.001) in smokers than those in nonsmokers. The %FMD and 8-isoprostane level did not change after passive smoking in smokers. In nonsmokers, however, the %FMD decreased (to 5.0% ± 1.9%, p < 0.001) and the 8-isoprostane level increased (to 37.8 ± 9.6 pg/mL, p < 0.001) significantly after 30 min passive smoking exposure, equivalently to the levels of smokers. Sixty corrected samples before and after passive smoking exposure in all patients showed a significant negative correlation between the % FMD and the plasma 8-isoprostane levels (n = 60, r = –0.69, p < 0.001). Even 30 min of passive smoking rapidly impairs vascular endothelial function, which is associated with oxidative stress. Our data provide the pathophysiological insight for the recent epidemiological evidence about the increased risk of coronary heart disease among nonsmokers exposed to passive smoking.


2005 ◽  
Vol 164 (12) ◽  
pp. 775-778 ◽  
Author(s):  
Ali Aycicek ◽  
Ozcan Erel ◽  
Abdurrahim Kocyigit

2014 ◽  
Vol 454 (1) ◽  
pp. 131-136 ◽  
Author(s):  
Anastasios A. Theodorou ◽  
Vassilis Paschalis ◽  
Antonios Kyparos ◽  
George Panayiotou ◽  
Michalis G. Nikolaidis

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