Oxidative stress induction by short time exposure to ozone on THP-1 cells

Foucaud, Laurent; Bennasroune, Amar; Klestadt, Deborah; Laval-Gilly, Philippe; Falla, Jaı̈ro

doi:10.1016/j.tiv.2005.06.007

Cited by 18 publications

(10 citation statements)

References 43 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…O 3 is a very reactive gas whose uptake depends on the availability of antioxidants in the lining fluids, and its toxicity appears to be transmitted to the respiratory epithelium by secondary ROS formed by direct ozonisation of respiratory tract lining fluid lipids [16]. Alteration of the cell membrane translating an induction of lipid peroxidation and a significant modification of the redox status has been observed [53], as well as the activation of transcription factors such as NF-kB and increased expression of a range of pro-inflammatory cytokines and adhesion genes [2,6]. O 3 has been shown to react readily with ascorbic acid, uric acid and thiols, and exposure of these molecular species to O 3 results in their rapid depletion [6].…”

Section: Biological and Epidemiological Evidencementioning

confidence: 99%

“…O 3 has been shown to react readily with ascorbic acid, uric acid and thiols, and exposure of these molecular species to O 3 results in their rapid depletion [6]. When these defence mechanisms are overwhelmed, O 3 may injure the underlying cells by inducing lipid peroxidation and activating inflammatory gene expression [6,53]. Like O 3 , nitrogen dioxide (NO 2 ) reacts with substrates present in the lung lining fluid compartment.…”

Section: Biological and Epidemiological Evidencementioning

confidence: 99%

See 1 more Smart Citation

Air pollution, oxidative stress and dietary supplementation: a review

Romieu

Castro-Giner²,

Künzli³

et al. 2007

Eur Respir J

222

157

View full text Add to dashboard Cite

The aim of the present review was to provide an up-to-date overview of the biological and epidemiological evidence of the role of oxidative stress as a major underlying feature of the toxic effect of air pollutants, and the potential role of dietary supplementation in enhancing antioxidant defences.A bibliographic search was conducted through PubMed. The keywords used in the search were ''air pollutant'', ''oxidative stress'', ''inflammation'', ''antioxidant polyunsaturated fatty acids'' and ''genetics''. In addition, the authors also searched for biomarkers of oxidative stress and nutrients.The review presents the most recent data on: the biological and epidemiological evidence of the oxidative stress response to air pollutants; the role of dietary supplementation as a modulator of these effects; and factors of inter-individual variation in human response. The methodology for further epidemiological studies will be discussed in order to improve the current understanding on how nutritional factors may act.There is substantial evidence that air pollution exposure results in increased oxidative stress and that dietary supplementation may play a modulating role on the acute effect of air pollutants. Further epidemiological studies should address the impact of supplementation strategies in the prevention of air-pollution-related long-term effects in areas where people are destined to be exposed for the distant future.

show abstract

Section: Biological and Epidemiological Evidencementioning

confidence: 99%

Section: Biological and Epidemiological Evidencementioning

confidence: 99%

Air pollution, oxidative stress and dietary supplementation: a review

Romieu

Castro-Giner²,

Künzli³

et al. 2007

Eur Respir J

222

157

View full text Add to dashboard Cite

show abstract

“…GPx activity was determined in cell lysates with a RANSEL (RS505) reagent kit (Randox Laboratories; Garçon et al, 2001c;Paglia and Valentine, 1967). Total glutathione and glutathione disulfi de were determined in a recycling assay using 5,5-dithio-bis(2-nitrobenzoic acid) and glutathione reductase (Foucaud et al, 2006).…”

Section: Study Of Oxidative Stressmentioning

confidence: 99%

Oxidative damage induced in A549 cells by physically and chemically characterized air particulate matter (PM_2.5) collected in Abidjan, Côte d'Ivoire

Kouassi

Billet

Garçon

et al. 2009

J of Applied Toxicology

View full text Add to dashboard Cite

Exposure to high levels of air pollution particulate matter (PM) is strongly associated with increased pulmonary morbidity and mortality. However, the underlying mechanisms of action whereby PM cause adverse health effects are still unclear. In developing countries, like in the sub-Saharian region of Africa, people are often exposed to high PM levels. Hence, three PM(2.5) samples were collected in the District of Abidjan (Côte d'Ivoire), under rural, urban or industrial influences. Their most toxicologically relevant physical and chemical characteristics were determined--thereby showing that most of them were equal or smaller than 2.5 microm--and the influence of both natural (Ca, Na, Mg, Ti, etc.) and anthropic (Al, Fe, Mn, Cr, Pb, Zn, Cu, Ni, benzene and its derivatives, paraffins, etc.) emission sources. The toxicity induced by the three PM samples was studied through 5-bromodeoxyuridine incorporation to DNA, mitochondrial dehydrogenase activity and extracellular lactate dehydrogenase activity. Hence, effect concentrations at 10 and 50% (EC(10) and EC(50), respectively) were as follows: (i) rural PM--EC(10) = 5.91 microg cm(-2) and EC(50) = 29.55 microg cm(-2); (ii) urban PM--EC(10) = 5.45 microg cm(-2) and EC(50) = 27.23 microg cm(-2); and (iii) industrial PM--EC(10) = 6.86 microg cm(-2) and EC(50) = 34.29 microg cm(-2). Moreover, PM-induced oxidative damage in A549 cells was observed through the induction of lipid peroxidation, the alteration of superoxide dismutase activity, and the disruption of glutathione status. Both the transition metals and the organic chemicals within the three collected PM samples under study might be involved in the oxidative damage and, therefore, the toxicity they induced in A549 cells.

show abstract

“…Except for a 5-fold increase in heme oxygenase 1 (HMOX1), most statistically significant transcriptional changes were modest, with 2-fold or lower increases or decreases for all other genes analyzed, 23 of which are shown on Table 1. Among the genes up-regulated by VAN and CIN were HMOX1, a gene up-regulated in response to oxidative stress [38,39], and the heat shock 70 kDa protein 1B (HSPA1B). In addition, two genes in the glutathione synthesis pathway, GCLC and GCLM, were up-regulated after CIN exposure.…”

Section: Discussionmentioning

confidence: 99%

Antimutagenicity of cinnamaldehyde and vanillin in human cells: Global gene expression and possible role of DNA damage and repair

King

Shaughnessy

Mure

et al. 2007

Mutation Research/Fundamental and Molecular Mechanisms of Mutag

View full text Add to dashboard Cite

Vanillin (VAN) and cinnamaldehyde (CIN) are dietary flavorings that exhibit antimutagenic activity against mutagen-induced and spontaneous mutations in bacteria. Although these compounds were antimutagenic against chromosomal mutations in mammalian cells, they have not been studied for antimutagenesis against spontaneous gene mutations in mammalian cells. Thus, we initiated studies with VAN and CIN in human mismatch repair-deficient (hMLH1 − ) HCT116 colon cancer cells, which exhibit high spontaneous mutation rates (mutations/cell/generation) at the HPRT locus, permitting analysis of antimutagenic effects of agents against spontaneous mutation. Long-term (1-3-week) treatments of HCT116 cells with VAN at minimally toxic concentrations (0.5-2.5 mM) reduced the spontaneous HPRT mutant fraction (MF, mutants/10 6 survivors) in a concentrationrelated manner by 19% to 73%. A similar treatment with CIN at 2.5-7.5 μM yielded a 13% to 56% reduction of the spontaneous MF. Short-term (4-h) treatments also reduced the spontaneous MF by 64% (VAN) and 31% (CIN). To investigate the mechanisms of antimutagenesis, we evaluated the ability of VAN and CIN to induce DNA damage (comet assay) and to alter global gene expression (Affymetrix GeneChip) after 4-h treatments. Both VAN and CIN induced DNA damage in both mismatch repair-proficient (HCT116 + chr3) and deficient (HCT116) cells at concentrations that were antimutagenic in HCT116 cells. There were 64 genes in common whose expression was changed similarly by both VAN and CIN; these included genes related to DNA damage, stress responses, oxidative damage, apoptosis, and cell growth. RT-PCR results paralleled the Affymetrix results for 4 selected genes (HMOX1, DDIT4, GCLM, and CLK4). Our results show for the first time that VAN and CIN Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. These and other data lead us to propose that VAN and CIN may induce DNA damage that elicits recombinational DNA repair and, consequently, reduces spontaneous mutation. NIH Public Access

show abstract

Oxidative stress induction by short time exposure to ozone on THP-1 cells

Cited by 18 publications

References 43 publications

Air pollution, oxidative stress and dietary supplementation: a review

Air pollution, oxidative stress and dietary supplementation: a review

Oxidative damage induced in A549 cells by physically and chemically characterized air particulate matter (PM_2.5) collected in Abidjan, Côte d'Ivoire

Antimutagenicity of cinnamaldehyde and vanillin in human cells: Global gene expression and possible role of DNA damage and repair

Contact Info

Product

Resources

About

Oxidative stress induction by short time exposure to ozone on THP-1 cells

Cited by 18 publications

References 43 publications

Air pollution, oxidative stress and dietary supplementation: a review

Air pollution, oxidative stress and dietary supplementation: a review

Oxidative damage induced in A549 cells by physically and chemically characterized air particulate matter (PM2.5) collected in Abidjan, Côte d'Ivoire

Antimutagenicity of cinnamaldehyde and vanillin in human cells: Global gene expression and possible role of DNA damage and repair

Contact Info

Product

Resources

About

Oxidative damage induced in A549 cells by physically and chemically characterized air particulate matter (PM_2.5) collected in Abidjan, Côte d'Ivoire