scholarly journals The Role of Green Tea and Oxidative Stress in Heart Remodeling Induced by Tobacco Smoke Exposure

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Elenize Jamas Pereira ◽  
Marcos Minicucci ◽  
Bertha Polegato ◽  
Priscila Portugal ◽  
Diego Batista ◽  
...  
Clinics ◽  
2009 ◽  
Vol 64 (7) ◽  
Author(s):  
Daniella R. Duarte ◽  
Marcos F. Minicucci ◽  
Paula S. Azevedo ◽  
Beatriz B. Matsubara ◽  
Luiz S. Matsubara ◽  
...  

Life Sciences ◽  
2019 ◽  
Vol 227 ◽  
pp. 58-63 ◽  
Author(s):  
Nour A. Al-Sawalha ◽  
Karem H. Alzoubi ◽  
Omar F. Khabour ◽  
Weam Alyacoub ◽  
Yehya Almahmood

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.


2021 ◽  
pp. 1-7
Author(s):  
Oktay Aslaner

<b><i>Objective:</i></b> Cigarette smoking is a life-threatening habit that has rapidly spread in every socioeconomic part of the public worldwide. There exist mechanisms of nicotine delivery available to use in the hope of halting cigarette smoking, and the electronic cigarette (EC) is one of the common methods used for tobacco smoking replacement. This study aimed to investigate experimentally the oxidative effects of tobacco smoke and EC smoke which contain nicotine. <b><i>Method:</i></b> We constructed smoke circuit rooms for exposing the rats to EC or tobacco smoke. Three groups were created, the control group (<i>N</i> = 8); the electronic cigarette group (<i>N</i> = 8), exposure to electronic cigarette smoke for 2 h per day; and the tobacco group (<i>N</i> = 8), exposure to traditional cigarette smoke for 2 h per day. After the first and second week of exposure, blood samples were obtained, and serum oxidative stress index (OSI), paraoxonase 1 (PON1) activity, and prolidase levels were evaluated. <b><i>Results:</i></b> Higher values of OSI and prolidase levels were detected in the first week of EC or tobacco smoke exposure in both study groups (<i>p</i> &#x3c; 0.001) when compared with the control group, and partial decrements were observed in the second week. By contrast, elevated PON1 levels were observed in the second week after EC or tobacco smoke exposure. The highest OSI levels were observed in the tobacco smoke group (<i>p</i> &#x3c; 0.001). The lowest values of PON1 levels were detected in the first week of the electronic cigarette smoke group, and this decremental value was statistically different than normal, the second week of the electronic cigarette smoke group, the first week of the traditional cigarette smoke exposure group, and the second week of the traditional cigarette smoke exposure group values (<i>p</i> &#x3c; 0.000). <b><i>Conclusion:</i></b> Our results indicate that EC smoke induced oxidative stress. Therefore, ECs are potentially risky for human health and can lead to important health problems.


2012 ◽  
Vol 155 (3) ◽  
pp. 472-473 ◽  
Author(s):  
Bruna Paola Murino Rafacho ◽  
Priscila Santos ◽  
Heloisa Balan Assalin ◽  
Lidiane Paula Ardisson ◽  
Meliza Goi Roscani ◽  
...  

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