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CSE effect on ROS intracellular levels measured in 16-HBE cells. Examples of fluorescence microscopy original images. Each image represents a ROI (region of interest). Graphs represent the average of the mean fluorescence intensity measured in all ROIs, expressed as percentage of control condition (reported as %F compared to control (ROS intracellular levels) in the graphs) recorded in cells exposed to A) PBS (CTRL: control), 5% CSE, 5%CSE and 100 µM S-CMC-Lys (CSE + CMC) for 3 hours (n=70) . n is the number of ROIs. Scale bar = 100 µm. * = p < 0.05 with one-way Anova statistical analysis.
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Background: Cigarette smoke extract (CSE), a model for studying the effects of tobacco smoke in vivo and in vitro, induces cell oxidative stress and affects the antioxidative glutathione system. We evaluated the impact of CSE on airway epithelial cells and the possible cytoprotective effect of the mucolitic drug S-carboximethilcysteine lysine salt...
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... has been demonstrated that S-CMC-Lys may have a beneficial buffering effect on ROS concentration after the exposure to 5% CSE for 3 hours, that caused the maximal effects on cellular GSH levels, both in the presence and absence of S-CMC-Lys. We found that ROS intracellular levels, that were significantly increased after CSE exposure (Fig. 3), were reverted to a value comparable to the control in the presence of 100 µM ...
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Background:
Although exposure to cigarette smoking during pregnancy has been associated with alterations of DNA methylation in the cord blood or placental cells, whether such exposure before pregnancy could induce epigenetic alterations in the placenta of former smokers has never been investigated.
Methods:
Our approach combined the analysis of...
Citations
... The adaptive glutathione response consists of coordinated reactions during glutathione synthesis, utilization, recycling, and transport (Gould et al., 2015). Exposure to cigarette smoke has been reported to decrease glutathione levels and reduce the expression or activity of several antioxidant enzymes (Bazzini et al., 2013). This depletion may be directly related to increased lipid peroxidation, which could be attributed to increased ROS generation by cigarette smoking, in addition to uptake by the antioxidant enzyme glutathione. ...
Background: Smoking is associated with increased oxidative stress and inflammation, which can lead to the development of various diseases. Blood cotinine level is a reliable biomarker of nicotine exposure, and glutathione and malondialdehyde levels are biomarkers of oxidative stress and inflammation. Several studies have been conducted to investigate the relationship between blood cotinine levels, glutathione levels, and malondialdehyde levels in smokers. Therefore, we conducted this meta-analysis to investigate the association.
Methods: All cross-sectional and case-control studies published in the last 20 years (2003-2023) were identified by searching electronic databases such as PubMed, Science Direct, DOAJ, ResearchGate, and Google Scholar. Inclusion criteria were studies that focused on the relationship between blood cotinine levels, glutathione levels, and malondialdehyde levels in smokers, while qualitative research type, non-human studies, and studies that included variable measurement parameters saliva, urine, and hair were excluded.
Results: Six case-control and cross-sectional studies with 333 participants who were smokers and 267 participants who were non-smokers were included in the meta-analysis. There was a significant association between blood cotinine levels with malondialdehyde levels in smokers (MD = 115.37, p 0.0004, 95% CI = 51.92 to 178.82). The mean difference is positive indicating that the average blood levels of cotinine in smokers tend to be higher than malondialdehyde levels in smokers.
Conclusions: Based on our meta-analysis, blood cotinine levels were significantly associated with malondialdehyde levels in smokers. Smoking can increase blood cotinine levels of smokers compared with that of non-smokers.
... In addition, NQO1 and HO-1 also provide protection against ROS and ROS-mediated oxidative harm (Preethi et al., 2022). It has been observed that the exposure of CSE to cells can substantially upregulate the expression of gene encoding GPX-2 as a compensatory mechanism for protection against the cigarette smoke oxidant (Bazzini et al., 2013). Our study showed an increase in the expression of gene encoding GPX2 when exposed to 5% CSE; however, no significant reduction was observed in its expression with treatment of ZER-LCNs. ...
The purpose of this study was to evaluate the potential of zerumbone-loaded liquid crystalline nanoparticles (ZER-LCNs) in the protection of broncho-epithelial cells and alveolar macrophages against oxidative stress, inflammation and senescence induced by cigarette smoke extract in vitro. The effect of the treatment of ZER-LCNs on in vitro cell models of cigarette smoke extract (CSE)-treated mouse RAW264.7 and human BCi-NS1.1 basal epithelial cell lines was evaluated for their anti-inflammatory, antioxidant and anti-senescence activities using colorimetric and fluorescence-based assays, fluorescence imaging, RT-qPCR and proteome profiler kit. The ZER-LCNs successfully reduced the expression of pro-inflammatory markers including Il-6, Il-1β and Tnf-α, as well as the production of nitric oxide in RAW 264.7 cells. Additionally, ZER-LCNs successfully inhibited oxidative stress through reduction of reactive oxygen species (ROS) levels and regulation of genes, namely GPX2 and GCLC in BCi-NS1.1 cells. Anti-senescence activity of ZER-LCNs was also observed in BCi-NS1.1 cells, with significant reductions in the expression of SIRT1, CDKN1A and CDKN2A. This study demonstrates strong in vitro anti-inflammatory, antioxidative and anti-senescence activities of ZER-LCNs paving the path for this formulation to be translated into a promising therapeutic agent for chronic respiratory inflammatory conditions including COPD and asthma.
... Meanwhile, an in vitro study by Kimura and co-workers [76] has revealed that primary human hepatocytes treated with 100 and 200 mM of ethanol showed the induction of GCLC gene expression via the activation of the NF-κB pathway. Tobacco smoking is also well known to deplete glutathione [77][78][79]. Thus, our study supports the causative roles of tobacco smoking and alcohol abuse in the development of psoriasis, and the negative effects of these environmental factors eliminate the protective role of polymorphisms of the GCLC gene against disease risk. ...
The aim of this pilot study was to investigate whether single nucleotide polymorphisms (SNP) in the gene encoding the catalytic subunit of glutamate cysteine ligase (GCLC) are associated with the risk and clinical features of psoriasis. A total of 944 unrelated individuals, including 474 patients with a diagnosis of psoriasis and 470 healthy controls, were recruited for the study. Six common SNPs in the GCLC gene were genotyped using the MassArray-4 system. Polymorphisms rs648595 (OR = 0.56, 95% CI 0.35–0.90; Pperm = 0.017) and rs2397147 (OR = 0.54, 95% CI 0.30–0.98; Pperm = 0.05) were associated with susceptibility to psoriasis in males. In the male group, diplotype rs2397147-C/C × rs17883901-G/G was associated with a decreased risk of psoriasis (FDR-adjusted p = 0.014), whereas diplotype rs6933870-G/G × rs17883901-G/G (FDR-adjusted p = 0.045) showed an association with an increased disease risk in females. The joint effects of SNPs with tobacco smoking (rs648595 and rs17883901) and alcohol abuse (rs648595 and rs542914) on psoriasis risk were observed (Pperm ≤ 0.05). We also found multiple sex-independent associations between GCLC gene polymorphisms and various clinical features such as earlier disease onset, the psoriatic triad, and specific localizations of skin lesions. The present study is the first to show that polymorphisms of the GCLC gene are significantly associated with the risk of psoriasis and related to its clinical features.
... Meanwhile, in vitro study by Kimura and coworkers [76] has revealed that primary human hepatocytes treated with 100 and 200 mM ethanol were found to induce transcriptional activity of the GCLC gene through the activation of the NF-κB pathway. Tobacco smoking is also well known to deplete glutathione [77,78,79]. Thus, our study supports the causative roles of tobacco smoking and alcohol abuse in the development of psoriasis, and the negative effects of these environmental factors eliminate the protective role of polymorphisms of the GCLC gene against disease risk. ...
The aim of this pilot study was to investigate whether single nucleotide polymorphisms (SNP) in the gene encoding the catalytic subunit of glutamate cysteine ligase (GCLC) are associated with the risk and clinical features of psoriasis. A total of 944 unrelated individuals, including 474 patients with a diagnosis of psoriasis and 470 healthy controls, were recruited for the study. Six common SNPs in the GCLC gene were genotyped using the MassArray-4 system. Polymorphisms rs648595 (OR=0.56 95%CI 0.35-0.90, Pperm=0.017) and rs2397147 (OR=0.54 95%CI 0.30-0.98, Pperm=0.05) were associated with susceptibility to psoriasis in males. In the male group, diplotype rs2397147-C/C×rs17883901-G/G was associated with decreased risk of psoriasis (FDR-adjusted P=0.014), whereas diplotype rs6933870-G/G×rs17883901-G/G (FDR-adjusted P=0.045) showed association with increased disease risk in females. Joint effects of SNPs with tobacco smoking (rs648595 and rs17883901) and alcohol abuse (rs648595 and rs542914) on the risk of psoriasis were observed (Pperm≤0.05). Furthermore, we found multiple sex-independent associations between GCLC gene polymorphisms and various clinical features such as earlier disease onset, the psoriatic triad, and specific localizations of skin lesions. The present study is the first to show that polymorphisms of the GCLC gene are significantly associated with the risk of psoriasis and related to its clinical features.
... Exposure to chronic cigarette smoke can reduce GSH levels in ELF, plasma, and lungs after the GSH adaptive response period is exceeded. [18][19][20] Previous studies have shown that supplementation with vitamins C and E is expected to reduce the harmful effects of cigarettes. The effectiveness of most antioxidants is generally seen in proportion to the number of hydroxyls (OH) groups present in the aromatic ring so that natural substances appear to have better antioxidant activity than synthetic antioxidants. ...
Background: Cigarette smoke can trigger oxidative stress. An alternative to overcome the harmful effects of cigarette smoke is through antioxidants. White oyster mushrooms ( Pleurotus Ostreatus ostreatus or P. ostreatus ) are a source of exogenous antioxidants because many contain active compounds for potential antioxidants such as phenol and flavonoid compounds. The purpose of this study was to analyze the effect of ethanolic extract of Pleurotus P. ostreatus on 4-hydroxy-2-nonenal (HNE) and glutathione (GSH), as well as to analyze their correlation in the lung of Wistar male rats exposed to cigarette smoke.
Methods: The study was a preclinical experiment conducted on 24 rats divided into four groups. The treatment was carried out for 42 days and antioxidant effects were assessed through levels of HNE and GSH in rat lungs. Groups were divided as follows: I- normal control, II- negative control, III and IV exposed to cigarette smoke for 60 minutes/day. Group III (treatment group) was treated with ethanolic extract of Pleurotus P. ostreatus at 250 mg/kg BW rat/day, and group IV (comparison group) was treated with N-acetyl cysteine 600 mg /day. Data analysis used was one-way ANOVA and Kruskal Wallis test, and Spearmen rank correlation coefficient test.
Results: The results showed that the group receiving ethanolic extract of Pleurotus P. ostreatus had HNE levels of (44,18 ± 2,09 pg/mL) and GSH (0,04 ± 0,00 pg/mL) protein. This extract significantly increased GSH levels and inhibited the increase of HNE levels. Results of GSH (p≤0.01) showed significant results using one-way ANOVA.
Conclusions: The ethanolic extract of P. ostreatus can prevent lipid peroxidation and decrease endogenous antioxidant levels in lung cells exposed to cigarette smoke. Ethanolic extract of Pleurotus P. ostreatus has good antioxidant potential.
... In parallel, the expression of glutathione peroxidases 2 and 3, glutathione reductase, and glutamate-cysteine ligase is increased. Carbocysteine is effective in counteracting all of these effects [38]. With regard to cell apoptosis, Yoshida et al. demonstrated that carbocysteine reduces the increased cell apoptosis (caspase (CASP)3 and CASP9 activation) in tracheal epithelial cells exposed to H 2 O 2 [39]. ...
Chronic obstructive pulmonary disease (COPD) is a heterogeneous disease with a versatile and complicated profile, being the fourth most common single cause of death worldwide. Several research groups have been trying to identify possible therapeutic approaches to treat COPD, such as the use of mucoactive drugs, which include carbocysteine. However, their role in the treatment of patients suffering from COPD remains controversial due to COPD’s multifaceted profile. In the present review, 72 articles, published in peer-reviewed journals with high impact factors, are analyzed in order to provide significant insight and increase the knowledge about COPD considering the important contribution of carbocysteine in reducing exacerbations via multiple mechanisms. Carbocysteine is in fact able to modulate mucins and ciliary functions, and to counteract viral and bacterial infections as well as oxidative stress, offering cytoprotective effects. Furthermore, carbocysteine improves steroid responsiveness and exerts anti-inflammatory activity. This analysis demonstrates that the use of carbocysteine in COPD patients represents a well-tolerated treatment with a favorable safety profile, and might contribute to a better quality of life for patients suffering from this serious illness.
... However, scientific studies have also suggested that cells undergoing oxidative stress induced by CSE increase the expression of antioxidant genes as a cytoprotective response [46]. Bazzini et al. have shown that 24 h exposure of 5% CSE to 16HBE cells increases the Gpx2 gene expression more than 3.5 fold (compared to CSE-untreated control) and this increase in Gpx2 may be associated with a tolerance to cigarette smoking as a compensatory mechanism to combat cigarette-smoke oxidant [47]. In our study, we observed a 4.6-fold increase in Gpx2 gene expression in 16HBE cells after 24 h exposure to 5% CSE compared to untreated control, while treatment of BBR-LCNs reduced (but not significantly) Gpx2 expression compared to 5% CSE. ...
Cigarette smoke is considered a primary risk factor for chronic obstructive pulmonary disease. Numerous toxicants present in cigarette smoke are known to induce oxidative stress and airway inflammation that further exacerbate disease progression. Generally, the broncho-epithelial cells and alveolar macrophages exposed to cigarette smoke release massive amounts of oxidative stress and inflammation mediators. Chronic exposure of cigarette smoke leads to premature senescence of airway epithelial cells. This impairs cellular function and ultimately leads to the progression of chronic lung diseases. Therefore, an ideal therapeutic candidate should prevent disease progression by controlling oxidative stress, inflammation, and senescence during the initial stage of damage. In our study, we explored if berberine (an alkaloid)-loaded liquid crystalline nanoparticles (berberine-LCNs)-based treatment to human broncho-epithelial cells and macrophage inhibits oxidative stress, inflammation, and senescence induced by cigarette-smoke extract. The developed berberine-LCNs were found to have favourable physiochemical parameters, such as high entrapment efficiency and sustained in vitro release. The cellular-assay observations revealed that berberine-LCNs showed potent antioxidant activity by suppressing the generation of reactive oxygen species in both broncho-epithelial cells (16HBE) and macrophages (RAW264.7), and modulating the genes involved in inflammation and oxidative stress. Similarly, in 16HBE cells, berberine-LCNs inhibited the cigarette smoke-induced senescence as revealed by X-gal staining, gene expression of CDKN1A (p21), and immunofluorescent staining of p21. Further in-depth mechanistic investigations into antioxidative, anti-inflammatory, and antisenescence research will diversify the current findings of berberine as a promising therapeutic approach for inflammatory lung diseases caused by cigarette smoking.
... An in-depth analysis of the literature has led us to the assumption that endogenous glutathione deficiency may be a shared condition that occurs as a result of the influence of these risk factors. This assumption is based on the fact that chronic stress, alcohol abuse, and smoking might be responsible for the depletion of glutathione [63][64][65][66][67][68], whereas moderate physical activity and high levels of consumption of fresh vegetables and fruits contribute to an increase in endogenous biosynthesis of glutathione [69][70][71]. In particular, it is known that short-term emotional stress can cause positive changes in the activity of enzymes involved in the synthesis of glutathione [72]. ...
The purpose of this pilot study was to explore whether polymorphisms in genes encoding the catalytic (GCLC) and modifier (GCLM) subunits of glutamate-cysteine ligase, a rate-limiting enzyme in glutathione synthesis, play a role in the development of ischemic stroke (IS) and the extent of brain damage. A total of 1288 unrelated Russians, including 600 IS patients and 688 age- and sex-matched healthy subjects, were enrolled for the study. Nine common single nucleotide polymorphisms (SNPs) of the GCLC and GCLM genes were genotyped using the MassArray-4 system. SNP rs2301022 of GCLM was strongly associated with a decreased risk of ischemic stroke regardless of sex and age (OR = 0.39, 95%CI 0.24–0.62, p < 0.0001). Two common haplotypes of GCLM possessed protective effects against ischemic stroke risk (p < 0.01), but exclusively in nonsmoker patients. Infarct size was increased by polymorphisms rs636933 and rs761142 of GCLC. The mbmdr method enabled identifying epistatic interactions of GCLC and GCLM gene polymorphisms with known IS susceptibility genes that, along with environmental risk factors, jointly contribute to the disease risk and brain infarct size. Understanding the impact of genes and environmental factors on glutathione metabolism will allow the development of effective strategies for the treatment of ischemic stroke and disease prevention.
... In this case, the dyes are non-fluorescent when reduced, but become highly fluorescent upon oxidation. The most widely used dye is the 2 ,7 -dichlorofluorescin diacetate (DCFDA) that become oxidized into 2 ,7 -dichlorofluorescein (DCF) by intracellular ROS [11,14,22,26,28,29,32,33,35,42,45,50,68,72,[83][84][85][87][88][89]104]. Other commercially available fluorogenic probes are also available [13,24,69,80]. ...
... The oxidative status of the cell can also be evaluated by measuring reduced glutathione (GSH) levels, which are decreased under oxidative stress conditions. GSH is measured in cell lysates using spectrophotometry [25,26,28,31,33,41,53,84,85,89,97], liquid chromatography coupled to mass spectrometry (LC-MS) [97], enzymatic methods [51] and fluorescence [87]. Custom-made or commercially available kits can be used [42,44]. ...
... SOD or catalase enzymatic activities can be measured using commercially available colorimetric assays [11,25,28,29,31,32,34,44,45,70,71,77,83,112]. In bronchial epithelial cells exposed to CSE, the levels of SOD [25,[29][30][31]34,39,42,45,77,112], catalase [25,31,42,77] or GSH-Px [44,77,87] are significantly reduced. ...
Exposure of the airways epithelium to environmental insults, including cigarette smoke, results in increased oxidative stress due to unbalance between oxidants and antioxidants in favor of oxidants. Oxidative stress is a feature of inflammation and promotes the progression of chronic lung diseases, including Chronic Obstructive Pulmonary Disease (COPD). Increased oxidative stress leads to exhaustion of antioxidant defenses, alterations in autophagy/mitophagy and cell survival regulatory mechanisms, thus promoting cell senescence. All these events are amplified by the increase of inflammation driven by oxidative stress. Several models of bronchial epithelial cells are used to study the molecular mechanisms and the cellular functions altered by cigarette smoke extract (CSE) exposure, and to test the efficacy of molecules with antioxidant properties. This review offers a comprehensive synthesis of human in-vitro and ex-vivo studies published from 2011 to 2021 describing the molecular and cellular mechanisms evoked by CSE exposure in bronchial epithelial cells, the most used experimental models and the mechanisms of action of cellular antioxidants systems as well as natural and synthetic antioxidant compounds.
... More than 19.2% of students in Indonesia currently smoke and 66.2% are exposed to secondhand smoke in public spaces. 2 Cigarette smoke contains more than 4,700 chemical components, such as carbon monoxide, carbon dioxide, tar, nicotine, nitrogen oxides, hydrogen cyanide, ammonia, and formaldehyde. 1 Free radicals and reactive oxygen species (ROS) in cigarette smoke are contained in gas phase and tar phase. ...
Background: Cigarettes smokes are a great external source of free radicals. The negative effects of cigarette smoke exposure can be systemic and affect all body systems, including the reproductive. Male rats exposed to cigarette smoke have a risk of oxidative stress and sperm damage. This can be overcome with herbal antioxidants such as white oyster mushrooms (Pleurotus ostreatus).
Objective: This study aimed to examine the protective effect of ethanolic extract of white oyster mushroom against damage to sperm morphology of rats exposed to cigarette smoke.
Methods: This study is an experimental study using 40 rats which were divided into 5 groups. Group I (normal control), group II (negative control) were only given exposure of cigarette smoke, Grups III, IV and V (treatments groups 1, 2, and 3) were given exposure of cigarette smoke and ethanolic extract a dose of 125, 250, and 500 mg/Kg BW/day for 14 days. On the 15th day, the percentage normal rat sperm were calculated under a 400x magnification microscope.
Results: Normal sperm count in group I was 79% ± 0.79, group II was 39% ± 0.55, Grup III, IV and V were 56% ± 0.15, 65% ± 0.54 and 66% ± 0.21.
