The effects of ?,?-unsaturated aldehydes on hepatic thiols and thiol-containing enzymes

Cooper, Kathryn; Witz, Gisela; Witmer, Charlotte

doi:10.1016/0272-0590(92)90172-e

Cited by 29 publications

(10 citation statements)

References 29 publications

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“…Acrolein can act directly as an electrophilic compound to deplete nonprotein sulfhydryl groups/glutathione in the respiratory epithelium (146,147) or to inactivate metabolizing enzymes (148,149). Despite limited knowledge about cisactivating and trans-activating elements regulating MUC5AC expression, electrophiles are known to activate gene expression via a mechanism involving glutathione depletion and the production of ROS (150).…”

Section: Smoke-induced Mucin Expressionmentioning

confidence: 99%

Mucin Overproduction in Chronic Inflammatory Lung Disease

Hauber

Foley

Hamid

2006

Canadian Respiratory Journal

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H-P Hauber, SC Foley, Q Hamid. Mucin overproduction in chronic inflammatory lung disease. Can Respir J 2006;13(6):327-335.Mucus overproduction and hypersecretion are commonly observed in chronic inflammatory lung disease. Mucins are gel-forming glycoproteins that can be stimulated by a variety of mediators. The present review addresses the mechanisms involved in the upregulation of secreted mucins. Mucin induction by neutrophil elastase, bacteria, cytokines, growth factors, smoke and cystic fibrosis transmembrane conductance regulator malfunction are also discussed.Key Words: Bacteria; Cytokine; Lung; Mucin; Neutrophil elastase; Overproduction; Smoke La surproduction de mucine dans la pneumopathie inflammatoire chronique La surproduction de mucus et l'hypersécrétion sont courantes en présence d'une pneumopathie inflammatoire chronique. Les mucines sont des glycoprotéines gélifiantes qui peuvent être stimulées par divers médiateurs. La présente analyse traite des mécanismes de régulation positive des mucines sécrétées. Est également exposée l'induction des mucines par l'élastase des neutrophiles, les bactéries, les cytokines, les facteurs de croissance, la fumée et la défaillance du régulateur de conductance transmembraneuse de la fibrose kystique. M ucus is an important component of both the physiological and pathological processes in airways. It protects, moisturizes and lubricates mucosal surfaces, and traps bacteria and other inhaled irritants for removal by mucociliary clearance. However, excessive production of airway mucus is a feature of chronic inflammatory lung diseases such as bronchial asthma, chronic obstructive pulmonary disease (COPD), bronchiectasis and cystic fibrosis (CF). Mucus hypersecretion results from hyperplasia and metaplasia of mucous cells, which lead to greater numbers of these cells being found throughout the airways, including the distal airways, where they are normally absent (1). The presence of neutrophil elastase, certain bacterial pathogens and altered cytokine patterns all contribute to excess airway mucus production. This overproduction and hypersecretion of mucus, in turn, contributes to airway obstruction and impairment of mucociliary clearance.An understanding of the mechanisms that lead to mucus overproduction and secretion is therefore of great clinical interest. The present review provides insight into the mechanisms by which excessive mucus production is stimulated in chronic inflammatory lung disease, focusing mainly on enhanced gene expression and protein production of secretory mucins in the airways. MUCINSMucus is formed within the airways by a polymeric matrix of large, oligomeric, gel-forming glycoproteins, called mucins. These gel-forming mucins are primarily responsible for the rheological properties of airway mucus (2). However, in disease states such as CF and chronic bronchitis, polymeric DNA and filamentous actin, two products of leukocyte lysis, contribute greatly to, and are the principal determinants of, the viscoelastic properties of the purulent sputum...

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Section: Smoke-induced Mucin Expressionmentioning

confidence: 99%

Mucin Overproduction in Chronic Inflammatory Lung Disease

Hauber

Foley

Hamid

2006

Canadian Respiratory Journal

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“…In different cell lines, a complete GSH depletion was observed from 10 mM acrolein [8][9][10][11]. After intraperitoneal administration of 5 mg acrolein/kg bw the GSH content in the liver of rats was reduced by approximately 50% [12].…”

Section: Introductionmentioning

confidence: 98%

Toxicology and risk assessment of acrolein in food

Abraham

Andres

Palavinskas

et al. 2011

Molecular Nutrition Food Res

150

126

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Acrolein is an α,β-unsaturated aldehyde formed by thermal treatment of animal and vegetable fats, carbohydrates and amino acids. In addition it is generated endogenously. As an electrophile, acrolein forms adducts with gluthathione and other cellular components and is therefore cytotoxic. Mutagenicity was shown in some in vitro tests. Acrolein forms different DNA adducts in vivo, but mutagenic and cancerogenous effects have not been demonstrated for oral exposure. In subchronic oral studies, local lesions were detected in the stomach of rats. Systemic effects have not been reported from basic studies. A WHO working group established a tolerable oral acrolein intake of 7.5 μg/kg body weight/day. Acrolein exposure via food cannot be assessed due to analytical difficulties and the lack of reliable content measurements. Human biomonitoring of an acrolein urinary metabolite allows rough estimates of acrolein exposure in the range of a few μg/kg body weight/day. High exposure could be ten times higher after the consumption of certain foods. Although the estimation of the dietary acrolein exposure is associated with uncertainties, it is concluded that a health risk seems to be unlikely.

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“…In this context, it has recently been reported that following exposure to cigarette smoke, cultured pulmonary artery endothelial cells generate superoxide anion (O 2 factors to trigger the generation of O 2 − (15,16). Such stable substances could be carried throughout the systemic circulation and act in organs remote to the lungs to stimulate ROS generation (17).…”

Section: Introductionmentioning

confidence: 99%

Nicotine- and Tar-Free Cigarette Smoke Induces Cell Damage Through Reactive Oxygen Species Newly Generated by PKC-Dependent Activation of NADPH Oxidase

et al. 2012

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Abstract.We examined cytotoxic effects of nicotine/tar-free cigarette smoke extract (CSE) on C6 glioma cells. The CSE induced plasma membrane damage (determined by lactate dehydrogenase leakage and propidium iodide uptake) and cell apoptosis {determined by MTS [3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium] reduction activity and DNA fragmentation}. The cytotoxic activity decayed with a half-life of approximately 2 h at 37°C, and it was abolished by N-acetyl-L-cysteine and reduced glutathione. The membrane damage was prevented by catalase and edaravone (a scavenger of• OH) but not by superoxide dismutase, indicating involvement of • OH. In contrast, the CSE-induced cell apoptosis was resistant to edaravone and induced by authentic H 2 O 2 or O 2 − generated by the xanthine/xanthine oxidase system, indicating involvement of H 2 O 2 or O 2 − in cell apoptosis. Diphenyleneiodonium [NADPH oxidase (NOX) inhibitor] and bisindolylmaleimide I [BIS I, protein kinase C (PKC) inhibitor] abolished membrane damage, whereas they partially inhibited apoptosis. These results demonstrate that 1) a stable component(s) in the CSE activates PKC, which stimulates NOX to generate reactive oxygen species (ROS), causing membrane damage and apoptosis; 2) different ROS are responsible for membrane damage and apoptosis; and 3) part of the apoptosis is caused by oxidants independently of PKC and NOX.[Supplementary methods and Figure: available only at http://dx

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The effects of ?,?-unsaturated aldehydes on hepatic thiols and thiol-containing enzymes

Cited by 29 publications

References 29 publications

Mucin Overproduction in Chronic Inflammatory Lung Disease

Mucin Overproduction in Chronic Inflammatory Lung Disease

Toxicology and risk assessment of acrolein in food

Nicotine- and Tar-Free Cigarette Smoke Induces Cell Damage Through Reactive Oxygen Species Newly Generated by PKC-Dependent Activation of NADPH Oxidase

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