Effect of Cigarette Smoking on the Oxidant/Antioxidant Balance in Healthy Subjects

Chávez, Jennifier; Cano, Clímaco; Souki, Aida; Bermúdez, Valmore; Medina, Mayerlim; Ciszek, Ana; Amell, Anilsa; Vargas, María Eugenia Bozzoli; Reyna, Nadia; Toledo, Abdon; Cano, Raquel; Suárez, Gustavo; Contreras, Freddy; Israili, Zafar H.; Hernández-Hernández, Rafael; Valasco, Manuel

doi:10.1097/01.psp.0000249918.19016.f6

Cited by 46 publications

(33 citation statements)

References 32 publications

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“…Several investigators have reported that oxidant reactions induced by cigarette smoke are related to the development of cardiovascular disease [38][39][40]. The present study did not investigate if the observed complement activation was due to tobacco smoke-induced oxidant damage to EC.…”

Section: Discussionmentioning

confidence: 70%

Regulated complement deposition on the surface of human endothelial cells: Effect of tobacco smoke and shear stress

Yin

Ghebrehiwet

Weksler

et al. 2008

Thrombosis Research

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Cigarette smoke and hemodynamic stress both contribute to vascular inflammation and associated atherosclerosis. We recently demonstrated direct activation of complement components C4 and C3 on human endothelial cells (EC). The present study was designed to explore complement activation on bone marrow microvascular endothelial cells (BMEC) and human umbilical vein endothelial cells (HUVEC) in response to endothelial cell injury by tobacco smoke extract, shear stress, or other known inflammatory and atherogenic mediators, lipopolysaccharide (LPS) and INF-γ. Following treatment, confluent EC monolayers were exposed to plasma (60 min, 37 °C), and cell surface deposition of stable complement derivatives C4d, iC3b and SC5b-9 was measured in situ using an ELISA approach. Consistent with previous results, moderate levels of C4d, iC3b and SC5b-9 deposition were observed on native EC monolayers exposed to human plasma. Tobacco smoke and shear stress enhanced EC C4d deposition. In contrast, LPS and INF-γ failed to affect EC mediated complement activation, despite evidence of EC activation illustrated by ICAM-1 expression. The combination of tobacco smoke and shear stress nearly doubled EC C4d expression. No increases in iC3b or SC5b-9 were noted, suggesting inhibition of classical and alternative pathway C3 convertase assembly or activity. Indeed, concomitantly increased surface expression of complement regulatory proteins CD35 (CR1) and CD55 was observed following EC exposure to tobacco smoke and shear stress. These results suggest that a balance between complement activation and regulation exists at the EC surface, and may impact vascular injury leading to thrombosis, arteriosclerosis, and atherogenesis.

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Section: Discussionmentioning

confidence: 70%

Regulated complement deposition on the surface of human endothelial cells: Effect of tobacco smoke and shear stress

Yin

Ghebrehiwet

Weksler

et al. 2008

Thrombosis Research

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“…An association between the Pon1 55 and Pon1 192 polymorphisms and coPD has not been studied according to our best knowledge. But, there are some studies on Pon1 activity in coPD (2,4,10,11,21).…”

Section: Resultsmentioning

confidence: 99%

“…in the recent years, several studies have showed that extracts of cigarette smoke inhibited the activity of Pon1 (2,9,21).…”

Section: Introductionmentioning

confidence: 99%

Chronic Obstructive Pulmonary Disease and Paraoxonase-1 192 and 55 Gene Polymorphisms

Tekes

Işık

Yıldız

et al. 2010

Biotechnology & Biotechnological Equipment

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“…These toxic substances in the cigarette smoke, such as tar, nicotine, lead, carbon monoxide, nitrogen monoxide, benzopyrene, and nitrosamines, will subsequently be metabolized in the liver to yield oxidants or free radicals. (14,18) Long-term and continual smoking leads to accumulation of these toxic substances in the body, so that there is an increase in free radicals, such as hydroxyl and superoxide radicals. The increase in free radicals causes an increase in oxidant markers such as MDA and a decrease in antioxidant markers such as GSH, glutathione peroxidase, catalase, and superoxide dismutase.…”

Section: Discussionmentioning

confidence: 99%

“…In contrast, a study on thirty healthy adult subjects (15 smokers and 15 nonsmokers) showed no significant changes in GSH and MDA concentrations of smokers. (14) In view of the large numbers of smokers in Indonesia particularly among university students and the differing results of previous studies, it was felt necessary to conduct another study on the association of smoking with MDA and GSH concentrations in smokers.…”

Section: Introductionmentioning

confidence: 99%

Smoking tends to decrease glutathione and increase malondialdehyde levels in medical students

Safyudin

Subandrate

2016

UnivMed

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Background Smoking is the act of introducing toxic substances into the body. Cigarette smoke contains chemicals that may cause several disorders, including cardiovascular disease, cancer, and chronic obstructive pulmonary disease. Toxic substances in cigarette smoke have the potential to increase free radicals, malondialdehyde (MDA) levels and to decrease endogenous antioxidant (glutathione/GSH) levels. This study aims to determine the relationship of smoking with plasma GSH and MDA levels in medical students. Methods This study was analytical observational with cross-sectional approach. The study was conducted from April to December 2015. The subjects in this study were medical students, consisting of 20 smokers and 20 nonsmokers. Plasma GSH and MDA levels were determined biochemically using Sigma GSH Assay Kit and Sigma MDA Assay Kit. Data was analyzed using the independent t test. Results The results showed that there was no significant difference between mean GSH in smokers (1.74 ± 0.91 mmol/L) and nonsmokers (2.42 ± 1.19 µmol/L) (p=0.441). Mean smokers MDA level of 2.06 ± 1.39 nmol/mL was not significantly different compared with mean nonsmokers MDA level (1.32 ± 0.90 nmol/mL) (p=0.092). Conclusions Smoking tends to decrease plasma GSH levels and increase plasma MDA levels in medical students. Smoking history could be evidence of oxidative stress and an impaired oxidant defense system. In particular, young smokers should quit promptly before health problems arise, so as to have the optimal benefits of cessation.

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Effect of Cigarette Smoking on the Oxidant/Antioxidant Balance in Healthy Subjects

Cited by 46 publications

References 32 publications

Regulated complement deposition on the surface of human endothelial cells: Effect of tobacco smoke and shear stress

Regulated complement deposition on the surface of human endothelial cells: Effect of tobacco smoke and shear stress

Chronic Obstructive Pulmonary Disease and Paraoxonase-1 192 and 55 Gene Polymorphisms

Smoking tends to decrease glutathione and increase malondialdehyde levels in medical students

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