scholarly journals Resistin as a Prooxidant Factor and Predictor of Endothelium Damage in Patients with Mild Acute Pancreatitis Exposed to Tobacco Smoke Xenobiotics

2017 ◽  
Vol 2017 ◽  
pp. 1-10
Author(s):  
Milena Ściskalska ◽  
Grzegorz Marek ◽  
Zygmunt Grzebieniak ◽  
Halina Milnerowicz

Objectives. The study was aimed to assess the influence of tobacco smoke exposure on the intensity of inflammation measured by IL-6, α1-antitripsin (AAT) and α1-acid glycoprotein (AGP) concentrations, and Cd level and oxidative stress intensity measured by advanced oxidation protein product (AOPP) concentration in the blood of healthy subjects and AP patients during hospitalization. Endothelin-1 (ET-1) and resistin concentrations, markers of endothelium injury, were determined. Results. An increased IL-6 concentration in healthy smokers compared to nonsmokers and AP patients compared to controls was shown. An increased AAT and AGP concentrations during hospitalization of AP patients were noted, in both smokers (AAT, AGP) and nonsmokers (AAT). In comparison to control groups, in AP patients, a 2-fold increased resistin concentration correlating with ET-1 concentration and decreased albumin concentration accompanied by increased AOPP concentration were demonstrated. AOPP concentration was higher in smokers with AP compared to nonsmokers and gradually enhanced during their hospitalization. Conclusions. Tobacco smoke exposure can have a proinflammatory effect in both healthy subjects and AP patients. Increased resistin concentration in AP patients negatively correlating with albumin concentration has prooxidative effect on this protein resulting in enhanced AOPP level. Increased resistin concentration can intensify AAT and AGP production during AP.

BMC Cancer ◽  
2006 ◽  
Vol 6 (1) ◽  
Author(s):  
Renato B Fagundes ◽  
Christian C Abnet ◽  
Paul T Strickland ◽  
Farin Kamangar ◽  
Mark J Roth ◽  
...  

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Elenize Jamas Pereira ◽  
Marcos Minicucci ◽  
Bertha Polegato ◽  
Priscila Portugal ◽  
Diego Batista ◽  
...  

Andrologia ◽  
2019 ◽  
Vol 51 (8) ◽  
Author(s):  
Nour A. Al‐Sawalha ◽  
Yehya M. Almahmmod ◽  
Karem H. Alzoubi ◽  
Omar F. Khabour ◽  
Weam N. Alyacoub

2019 ◽  
Author(s):  
Jennifer A. Aguiar ◽  
Ryan D. Huff ◽  
Wayne Tse ◽  
Martin R. Stampfli ◽  
Brendan J. McConkey ◽  
...  

AbstractGlobal recreational cannabis use is a potentially important public health issue that would benefit from experimental evidence to inform policy, regulations, and individual user practices. Comparative analyses between cannabis and tobacco smoke, the latter long reported to have negative impacts on respiratory health, may help provide context and provide clinically relevant evidence.To address this unmet need we performed a comparative study between cannabis and tobacco smoke exposure in the Calu-3 human airway epithelial cells using concentration-response and pharmacological intervention study designs with outcome measurements of cell viability, epithelial cell barrier function, cytokine profile, and transcriptomics.Our results demonstrate that cannabis smoke exposure reduces epithelial cell barrier function without impacting cell viability, accompanied by a cytokine profile associated with inflammation (elevated IL-6 and IL-8), barrier repair (elevated TGF-α and PDGF-AA) and suppressed antiviral immunity (decreased IP-10 and RANTES). Transcriptomic analyses revealed a cannabis smoke induced signature associated with suppressed antiviral genes and induction of oncogenic and oxidative stress pathways. Similar trends were observed for tobacco smoke exposure. A formoterol/budesonide intervention was unable to prevent cannabis smoke-induced reductions in antiviral pathways or normalize induction of oncogenic and oxidative stress responses.Our results show striking similarities between cannabis and tobacco smoke exposure on impairing barrier function, suppressing antiviral pathways, potentiating of pro-inflammatory mediators, and inducing oncogenic and oxidative stress gene expression signatures. Furthermore, we demonstrate that an intervention with formoterol and budesonide is unable to completely normalized cannabisinduced responses. Collectively our data suggest that cannabis smoke exposure is not innocuous and may possess many of the deleterious properties of tobacco smoke, warranting additional studies to support public policy, government regulations, and individual user practices.


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