Relationship between smoking and total antioxidant status, total oxidant status, oxidative stress index, vit C, vit E

Karademirci, M. Merve; Kutlu, Ruhuşen; Kılınç, İbrahim

doi:10.1111/crj.12757

Cited by 49 publications

(33 citation statements)

References 10 publications

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“…A recent metaanalysis indicated that the proportion of patients with lung cancer who continue to smoke after diagnosis ranged from 6 to 83% [35]. Mechanisms behind the association between smoking and fibrin clot properties in cancer patients remain to be established; however, most likely increased oxidative stress contributes to our observation [36]. Oxidative stress reflected by 8-epi-prostaglandin F 2α was enhanced in heavy smokers compared to never-smokers and strongly correlated with impaired fibrin clot properties in the former group [34].…”

Section: Discussionmentioning

confidence: 75%

Altered fibrin clot properties in advanced lung cancer: strong impact of cigarette smoking

et al. 2019

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Background Dense fibrin networks resistant to lysis have been reported in patients at high risk of thromboembolism. Little is known about fibrin clot properties in cancer. We investigated fibrin clot properties and their determinants in patients with inoperable lung cancer. Methods We enrolled 150 patients with advanced lung cancer prior to therapy and 90 control subjects matched by age, sex, cardiovascular disease, and diabetes. Plasma clot permeability (K s), turbidimetric analysis of clot formation, clot lysis time (CLT), microparticle-associated tissue factor (MP-TF) activity, thrombin generation, and serum cotinine levels were determined. Results Lung cancer patients, compared with controls, formed at a faster rate (− 8.1% lag phase) denser plasma fibrin networks (− 27.2% K s) that displayed impaired lysis (+ 26.5% CLT), along with 19.5% higher MP-TF activity and 100% higher peak thrombin generated, also after adjustment for potential confounders. Cotinine levels were associated with fibrin maximum absorbance (r = 0.20, p = 0.016) and K s (r = − 0.50, p < 0.0001) in cancer patients. On multivariate regression analysis, an increase in cotinine levels was a predictor of low K s (the lower quartile, < 5.8 × 10 −9 cm 2 ; odds ratio = 1.21 per 10 ng/ml, 95% confidence interval 1.02-1.46), but not CLT. Conclusion Advanced lung cancer is associated with the prothrombotic plasma clot phenotype largely driven by smoking.

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Section: Discussionmentioning

confidence: 75%

Altered fibrin clot properties in advanced lung cancer: strong impact of cigarette smoking

et al. 2019

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“…CS contains oxidative gases, PAHs and particulate matter, which are known to lead to endothelial inflammation through oxidative stress and carbon monoxide, which strongly binds to hemoglobin and therefore causes hypoxia (Fig. 17) [208,209]. However, nicotine alone has the ability to stimulate dendritic cells and monocytes, with the concomitant release of pro-inflammatory cytokines [210].…”

Section: Discussionmentioning

confidence: 99%

Electronic cigarettes increase endothelial progenitor cells in the blood of healthy volunteers

et al. 2016

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“…A novel finding in our study is that simply incubating fresh whole blood from smokers for 7 h without any exogenous stimulus increases the levels of a number of pro-inflammatory cytokines/chemokines, the most robust being IL-8. This ex-vivo generation of proinflammatory cytokines may be related to the higher levels of oxidative stress reported in cigarette smokers 42,43 . Cigarette smoking generates many reactive species, which may overwhelm the antioxidant defense system.…”

Section: Smoking Alters Innate and Acquired Immune Responsesmentioning

confidence: 92%

“…Cigarette smoking generates many reactive species, which may overwhelm the antioxidant defense system. While low molecular weight antioxidants such as vitamin E and C have been reported to be lower in smokers 42 , blood glutathione levels are 8-10% higher 44 . It is thus possible that cigarette smokers produce a compensatory level of glutathione to maintain a comparable in vivo level of cytokines/chemokines to non-smokers.…”

Section: Smoking Alters Innate and Acquired Immune Responsesmentioning

confidence: 96%

The effect of smoking on chronic inflammation, immune function and blood cell composition

Elisia

Lam

Cho

et al. 2020

Sci Rep

122

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Smoking is the number one risk factor for cancer mortality but only 15–20% of heavy smokers develop lung cancer. It would, therefore, be of great benefit to identify those at high risk early on so that preventative measures can be initiated. To investigate this, we evaluated the effects of smoking on inflammatory markers, innate and adaptive immune responses to bacterial and viral challenges and blood cell composition. We found that plasma samples from 30 heavy smokers (16 men and 14 women) had significantly higher CRP, fibrinogen, IL-6 and CEA levels than 36 non-smoking controls. Whole blood samples from smokers, incubated for 7 h at 37 °C in the absence of any exogenous stimuli, secreted significantly higher levels of IL-8 and a number of other cytokines/chemokines than non-smokers. When challenged for 7 h with E. coli, whole blood samples from smokers secreted significantly lower levels of many inflammatory cytokines/chemokines. However, when stimulated with HSV-1, significantly higher levels of both PGE2 and many cytokines/chemokines were secreted from smokers’ blood samples than from controls. In terms of blood cell composition, red blood cells, hematocrits, hemoglobin levels, MCV, MCH, MCHC, Pct and RDW levels were all elevated in smokers, in keeping with their compromised lung capacity. As well, total leukocytes were significantly higher, driven by increases in granulocytes and monocytes. In addition, smokers had lower NK cells and higher Tregs than controls, suggesting that smoking may reduce the ability to kill nascent tumor cells. Importantly, there was substantial person-to person variation amongst smokers with some showing markedly different values from controls and others showing normal levels of many parameters measured, indicating the former may be at significantly higher risk of developing lung cancer.

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Relationship between smoking and total antioxidant status, total oxidant status, oxidative stress index, vit C, vit E

Abstract: The parameters of TAS, vitamin C and vitamin E were significantly higher in the non-smoker group than in the smoker group. The levels of TOS and OSI were higher in the smoker group. It is known that cigarette smoking leads to various diseases because of the free radicals it contains.

Cited by 49 publications

References 10 publications

Altered fibrin clot properties in advanced lung cancer: strong impact of cigarette smoking

Altered fibrin clot properties in advanced lung cancer: strong impact of cigarette smoking

Electronic cigarettes increase endothelial progenitor cells in the blood of healthy volunteers

The effect of smoking on chronic inflammation, immune function and blood cell composition

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