In vitro exposure of tobacco specific nitrosamines decreases the rat lung phospholipids by enhanced phospholipase A2 activity

Vijayaraj, Panneerselvam; Sivaprakasam, Chinnarasu; Varthini, Lakshmanaperumal Vishnu; Sarkar, Mary; Nachiappan, Vasanthi

doi:10.1016/j.tiv.2014.05.001

Cited by 14 publications

(10 citation statements)

References 52 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…With regard to this system of nicotine delivery, during 2011 Trehy and co‐workers documented that the composition of refill products varies considerably as a result it is difficult to fully evaluate the hazards related to electronic cigarette usage . The content of the aerosol generated from e‐cigarette is highly variable, not only among different products but also within different samples of the same e‐liquids . Therefore, we suggest that further work is required to better understand the impact of the spectrum of e‐cigarette products may have on pulmonary function.…”

Section: Resultsmentioning

confidence: 99%

“…For example, NNN and NNK are primary carcinogenic TSNAs that are present in cigarette smoke . Upon interaction with a surfactant film, these agents enhance phospholipid hydrolysis and subsequently reduce content within the alveolar space; an accompanied increase in lysophospholipid is also noted . Within the body, lysophospholipids are formed as a result of phospholipase A2 stereoselective hydrolysis of the ester linkage of phospholipids to release fatty acids and lysophospholipids .…”

Section: Resultsmentioning

confidence: 99%

See 1 more Smart Citation

The impact of cigarette/e‐cigarette vapour on simulated pulmonary surfactant monolayers under physiologically relevant conditions

Davies

Birkett

Kotwa

et al. 2017

Surface & Interface Analysis

View full text Add to dashboard Cite

The impact of cigarette/e-cigarette vapour on simulated pulmonary surfactant monolayers under physiologically relevant conditions http://researchonline.ljmu.ac.uk/5333/ Article LJMU has developed LJMU Research Online for users to access the research output of the University more effectively. Copyright © and Moral Rights for the papers on this site are retained by the individual authors and/or other copyright owners. Users may download and/or print one copy of any article(s) in LJMU Research Online to facilitate their private study or for non-commercial research. You may not engage in further distribution of the material or use it for any profit-making activities or any commercial gain. LJMU Research OnlineThe version presented here may differ from the published version or from the version of the record. Please see the repository URL above for details on accessing the published version and note that access may require a subscription. Deviation in pulmonary surfactant structure-function activity can impair airway patency and lead to respiratory 8 disorders. This novel study aims to evaluate the influence cigarette / e-cigarette vapour has on model 9 surfactant films located within a simulated pulmonary environment using a lung biosimulator. 10Chromatographic analysis confirmed that nicotine levels were consistent with the sampling regimen

show abstract

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

The impact of cigarette/e‐cigarette vapour on simulated pulmonary surfactant monolayers under physiologically relevant conditions

Davies

Birkett

Kotwa

et al. 2017

Surface & Interface Analysis

View full text Add to dashboard Cite

show abstract

“…Membrane phospholipid content is regulated by phospholipase hydrolysis. Correspondingly, both CS [76] and tobacco-specific nitrosamine [77] exposures decrease lung phospholipids (phosphatidylcholine, phosphatidylglycerol, and phosphatidylserine) by enhancing phospholipase A2 activity [29, 77]. Additional likely downstream mediators of injury include increased activation of phospholipase A2 neuro-inflammatory pathways, release of pro-oxidative arachidonic acid, and formation of 4-HNE-protein adducts in the brain [78, 79].…”

Section: Discussionmentioning

confidence: 99%

Cigarette Smoke-Induced Alterations in Frontal White Matter Lipid Profiles Demonstrated by MALDI-Imaging Mass Spectrometry: Relevance to Alzheimer’s Disease

Nunez

Kay

Krotow

et al. 2016

JAD

View full text Add to dashboard Cite

Background Meta-analysis has shown that smokers have significantly increased risks for Alzheimer’s disease (AD), and neuroimaging studies showed that smoking alters white matter (WM) structural integrity. Objective Herein, we characterize the effects of cigarette smoke (CS) exposures and withdrawal on WM myelin lipid composition using matrix assisted laser desorption and ionization-imaging mass spectrometry (MALDI-IMS). Methods Young adult male A/J mice were exposed to air (8 weeks; A8), CS (4 or 8 weeks; CS4, CS8), or CS8 followed by 2 weeks recovery (CS8 + R). Frontal lobe WM was examined for indices of lipid and protein oxidation and lipid profile alterations by MALDI-IMS. Lipid ions were identified by MS/MS with the LIPID MAPS prediction tools database. Inter-group comparisons were made using principal component analysis and R-generated heatmap. Results CS increased lipid and protein adducts such that higher levels were present in CS8 compared with CS4 samples. CS8 + R reversed CS8 effects and normalized the levels of oxidative stress. MALDI-IMS demonstrated striking CS-associated alterations in WM lipid profiles characterized by either reductions or increases in phospholipids (phosphatidylinositol, phosphatidylserine, phosphatidylcholine, or phosphatidylethanolamine) and sphingolipids (sulfatides), and partial reversal of CS’s inhibitory effects with recovery. The heatmap hierarchical dendrogram and PCA distinguished CS exposure, duration, and withdrawal effects on WM lipid profiles. Conclusion CS-mediated WM degeneration is associated with lipid peroxidation, protein oxidative injury, and alterations in myelin lipid composition, including shifts in phospholipids and sphingolipids needed for membrane integrity, plasticity, and intracellular signaling. Future goals are to delineate WM abnormalities in AD using MALDI-IMS, and couple the findings with MRI-mass spectroscopy to improve in vivo diagnostics and early detection of brain biochemical responses to treatment.

show abstract

“…Therefore, CSmediated reductions in hepatic phospholipid levels could impair insulin/IGF signaling as occurs with NNK exposure [27,28]. Of note is that tobacco-specific nitrosamines decrease lung phospholipids (phosphatidylcholine, phosphatidylglycerol, and phosphatidylserine) by enhancing phospholipase A2 activity [70]. Moreover, nitrosamineinduced reductions in phospholipids can be accompanied by increases in neutral lipids [71].…”

Section: Discussionmentioning

confidence: 99%

Tobacco Smoke-Induced Alterations in Hepatic Lipid Profiles Demonstrated by Imaging Mass Spectrometry

Tong¹,

Nunez²,

Yalçın³

et al. 2016

Mass Spectrom Purif Tech

View full text Add to dashboard Cite

To account for differences in susceptibility to alcoholic liver disease (ALD), tobacco smoking should be evaluated as a potential cofactor given the very high percentage of heavy drinkers also smoke, and the NNK tobacco-specific nitrosamine was shown to cause steatohepatitis and exacerbate molecular and biochemical effects of alcohol on the liver. Since one of the key factors linked to ALD progression is dysregulated lipid metabolism, we examined effects of cigarette smoke (CS) exposures on hepatic lipid profiles using matrix-assisted laser desorption and ionization imaging mass spectrometry (MALDI-IMS). Adult male A/J mice were exposed to air (8 weeks; A8), CS for 4 (CS4) or 8 (CS8) weeks; or CS8 with 2 weeks recovery (CS8+R). MALDI-IMS demonstrated broad CS-associated reductions in hepatic phospholipids that were partly ameliorated by short-term recovery. Principal component analysis revealed CSassociated shifts in phospholipid profiles that also partly normalized with recovery. Heatmaps demonstrated striking effects of CS with graded responses to exposure duration and recovery. Importantly, several of the CS-induced lipid profile alterations persisted after air recovery, suggesting that the responses had become permanent, whereas others worsened with CS exposure duration and were either sustained or revered with recovery.

show abstract

In vitro exposure of tobacco specific nitrosamines decreases the rat lung phospholipids by enhanced phospholipase A2 activity

Cited by 14 publications

References 52 publications

The impact of cigarette/e‐cigarette vapour on simulated pulmonary surfactant monolayers under physiologically relevant conditions

The impact of cigarette/e‐cigarette vapour on simulated pulmonary surfactant monolayers under physiologically relevant conditions

Cigarette Smoke-Induced Alterations in Frontal White Matter Lipid Profiles Demonstrated by MALDI-Imaging Mass Spectrometry: Relevance to Alzheimer’s Disease

Tobacco Smoke-Induced Alterations in Hepatic Lipid Profiles Demonstrated by Imaging Mass Spectrometry

Contact Info

Product

Resources

About