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hexanal/inflamación

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ArtículosEnsayos clínicosPatentes
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The cytotoxicity of aldehydes was studied using human primary bronchial epithelial cells (PBEC) cultured at the air-liquid interface (ALI) or under submerged conditions. PBEC were exposed for 30min via the air phase to acrolein (0.1-1mg/m3), crotonaldehyde (1.5-15mg/m3) or hexanal (22-221mg/m3) or

Aldehydes (nonanal and hexanal) in rat and human bronchoalveolar lavage fluid after ozone exposure.

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We hypothesized that exposure of healthy humans to ozone at concentrations found in ambient air causes both ozonation and peroxidation of lipids in lung epithelial lining fluid. Smokers (12) and nonsmokers (15) were exposed once to air and twice to 0.22 ppm ozone for four hours with exercise in an

Acute effects of exposure to hexanal vapors in humans.

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OBJECTIVE n-Hexanal is a major component in emissions from stored wood pellets. The production and use of wood pellets has increased dramatically. Our aim was to evaluate acute health effects of n-hexanal vapors. METHODS Twelve healthy volunteers were exposed to 0, 2, and 10 ppm n-hexanal for 2

Identification of novel cytokine biomarkers of hexanal exposure associated with pulmonary toxicity.

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We aimed to investigate whether exposure to low-molecular-weight saturated aliphatic aldehydes induces an airway inflammation related to lung toxicity. In previous studies, we identified that several aldehydes induced inflammatory responses through the secretion of pro-inflammatory cytokines. Here,

MicroRNA response of inhalation exposure to hexanal in lung tissues from Fischer 344 rats.

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In previous studies, we have investigated the relationships between environmental chemicals and health risk based on omics analysis and identified significant biomarkers. Our current findings indicate that hexanal may be an important toxicant of the pulmonary system in epigenetic insights. MicroRNA

Antioxidant transport modulates peripheral airway reactivity and inflammation during ozone exposure.

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We examined the effects of ozone (O(3)) and endogenous antioxidant transport on canine peripheral airway function, central airway function, epithelial integrity, and inflammation. Dogs were either untreated or pretreated with probenecid (an anion-transport inhibitor) and exposed for 6 h to 0.2

Down-regulation of the inflammatory response after short-term exposure to low levels of chemical vapours.

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To investigate the relation between signs and symptoms of irritation and biomarkers of inflammatory markers in blood in healthy volunteers exposed to different chemical vapours for 2 or 4 hours in an exposure chamber.

METHODS
The investigated chemicals

Chemical compositions and antioxidant/anti-inflammatory activities of steam distillate from freeze-dried onion ( Allium cepa L.) sprout.

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Freeze-dried onion sprout was steam-distilled, and the distillate was extracted with dichloromethane (volatile sample). Water sample I was obtained from the residual aqueous solution in the extractor. The filtrate and the methanol extract of filtrand from the residual aqueous solution in the steam

Effects of parenteral iron on inflammation and the myocardium in hemodialysis patients.

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Inflammation is a nontraditional cardiovascular risk factor in hemodialysis patients. This pilot study tested the hypothesis that intravenous iron adds to this inflammation by increasing oxidative stress. Secondly, we described the association between iron indices and myocardial structure and

Comparison between exhaled and sputum oxidative stress biomarkers in chronic airway inflammation.

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The aim of the present study was to compare aldehyde levels resulting from lipid peroxidation in exhaled breath condensate (EBC) and induced sputum (IS) supernatant of subjects with asthma and chronic obstructive pulmonary disease (COPD). Aldehydes (malondialdehyde (MDA), acrolein, n-hexanal (C6),

Ozone exposure increases aldehydes in epithelial lining fluid in human lung.

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We hypothesized that exposure of healthy humans to ozone causes both ozonation and peroxidation of lipids in lung epithelial lining fluid. Twelve smokers and 15 nonsmokers (eight lung function "responders" and seven "nonresponders") were exposed once to air and twice to 0. 22 ppm ozone for 4 h with

Aldehydic lipid peroxidation products derived from linoleic acid.

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Lipid peroxidation (LPO) processes observed in diseases connected with inflammation involve mainly linoleic acid. Its primary LPO products, 9-hydroperoxy-10,12-octadecadienoic acid (9-HPODE) and 13-hydroperoxy-9,11-octadecadienoic acid (13-HPODE), decompose in multistep degradation reactions. These

Oxidized lipoproteins including HDL and their lipid peroxidation products inhibit TNF-alpha secretion by THP-1 human macrophages.

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It has been established that oxidized LDL (ox-LDL) modifies cytokine secretion by macrophages, for example, by reducing tumor necrosis factor alpha (TNF-(alpha) m-RNA. However, little is known about the effects of oxidized high density lipoprotein (ox-HDL). This study reports the effects of ox-HDL
A headspace solid-phase microextraction (HS-SPME) procedure based on five commercialised fibres (85 μm polyacrylate - PA, 100 μm polydimethylsiloxane - PDMS, 65 μm polydimethylsiloxane/divinylbenzene - PDMS/DVB, 70 μm carbowax/divinylbenzene - CW/DVB and 85 μm carboxen/polydimethylsiloxane -

Detection of aldehydes in bronchoalveolar lavage of rats exposed to ozone.

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We report the detection of hexanal, heptanal, and nonanal in the bronchoalveolar lavage (BAL) of rats exposed to 0.5 to 10 ppm ozone with or without simultaneous 5% CO2. These three aldehydes primarily result from the Criegee ozonation of specific mono- or polyunsaturated fatty acids that are
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