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acetaldehyde/radang
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Immunogenic and inflammatory responses to citrullinated proteins are enhanced following modification with malondialdehyde-acetaldehyde adducts.
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Effects of acetaldehyde on human airway constriction and inflammation.
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The purpose of the present study was to determine the effects of acetaldehyde on airway smooth muscle constriction and inflammation. An oral ethanol provocation test was performed in Japanese asthmatics to measure pulmonary function, blood ethanol, acetaldehyde and histamine. Acetaldehyde
mRNA induction and cytokine release of inflammatory mediators during in vitro exposure of human nasal respiratory epithelia to acetaldehyde.
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Acetaldehyde has been shown to be cytotoxic and carcinogenic to the upper respiratory tract epithelium of rodents following long-term exposure. Most animal studies have concentrated on carcinogenicity and DNA-protein cross-link formation, while less is known about potential dose- and time-dependent
Antibodies to malondialdehyde-acetaldehyde modified low-density lipoprotein in patients with newly diagnosed inflammatory joint disease
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Objective:To assess antibodies to malondialdehyde-acetaldehyde-modified low-density lipoprotein (MAA-LDL) in patients with newly diagnosed inflammatory joint disease. Method: Patients with rheumatoid arthritis (RA), spondyloarthritis (SpA), and undifferentiated arthritis (UA),
Association of malondialdehyde-acetaldehyde (MAA) adducted proteins with atherosclerotic-induced vascular inflammatory injury.
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Atherosclerosis is a vascular injury characterized by elevated tissue levels of tumor necrosis factor-alpha (TNF-alpha), increased expression of endothelial cell adhesion molecules, and vascular wall inflammatory cell infiltration. Foam cells are associated with atherosclerotic plaque material, and
Malondialdehyde-acetaldehyde (MAA) adducted surfactant protein induced lung inflammation is mediated through scavenger receptor a (SR-A1).
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Co-exposure to cigarette smoke and alcohol leads to the generation of high concentrations of acetaldehyde and malondialdehyde in the lung. These aldehydes being highly electrophilic in nature react with biologically relevant proteins such as surfactant protein D (SPD) through a Schiff base reaction
Acetaldehyde prevents nuclear factor-kappa B activation and hepatic inflammation in ethanol-fed rats.
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Acetaldehyde has been proposed as one of the mediators of liver injury in alcoholic liver disease. We investigated whether increased acetaldehyde levels affected the development of alcoholic liver injury. Male Wistar rats were fed a liquid diet containing fish oil and ethanol by intragastric
Acetaldehyde accumulation suppresses Kupffer cell release of TNF-Alpha and modifies acute hepatic inflammation in rats.
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BACKGROUND
Alcohol-related diseases have multiple and varied associations with acetaldehyde, a highly toxic product of ethanol oxidation that accumulates in the absence of active aldehyde dehydrogenase (ALDH). This study was designed to clarify the role of acetaldehyde in liver injury, specifically
Plasma IgA antibody levels to malondialdehyde acetaldehyde-adducts are associated with inflammatory mediators, obesity and type 2 diabetes.
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OBJECTIVE
Obesity and type 2 diabetes (T2D) associate with increased oxidative stress. Malondialdehyde acetaldehyde (MAA) adducts have been suggested to be one of the antigenic epitopes in MDA-LDL responsible for the antibody recognition. Our aim was to investigate the associations between plasma
Malondialdehyde-acetaldehyde (MAA) modified proteins induce pro-inflammatory and pro-fibrotic responses by liver endothelial cells.
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Effects of carbamazepine on plasma extravasation and bronchoconstriction induced by substance P, capsaicin, acetaldehyde and histamine in guinea-pig lower airways.
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We evaluated the in vivo effects of the pretreatment with carbamazepine (CBZ) at different doses (10, 20 and 40 mg/kg p.o.) on the Evans-blue extravasation and on bronchoconstriction induced by different substances in guinea-pig tracheal tissue. The drug dose-dependently inhibited the extravasation
Malondialdehyde-acetaldehyde adducts decrease bronchial epithelial wound repair.
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Most people who abuse alcohol are cigarette smokers. Previously, we have shown that malondialdehyde, an inflammation product of lipid peroxidation, and acetaldehyde, a component of both ethanol metabolism and cigarette smoke, form protein adducts that stimulate protein kinase C (PKC) activation in
Malondialdehyde-acetaldehyde (MAA) adducted proteins bind to scavenger receptor A in airway epithelial cells.
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Co-exposure to cigarette smoke and ethanol generates malondialdehyde and acetaldehyde, which can subsequently lead to the formation of aldehyde-adducted proteins. We have previously shown that exposure of bronchial epithelial cells to malondialdehyde-acetaldehyde (MAA) adducted protein increases
Sequential acetaldehyde production, lipid peroxidation, and fibrogenesis in micropig model of alcohol-induced liver disease.
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The pathogenesis of alcohol-induced liver disease involves the adverse effects of ethanol metabolites and oxidative tissue injury. Previous studies indicated that covalent protein adducts with reactive aldehydes may be formed in alcohol consumers. To study the role of such protein adducts in the
Ethanol causes inflammation in the airways by a neurogenic and TRPV1-dependent mechanism.
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Ethanol (EtOH) stimulates peptidergic primary sensory neurons via the activation of the transient receptor potential vanilloid-1 (TRPV1). EtOH is also known to trigger attacks of asthma in susceptible individuals. Our aim was to investigate whether EtOH produces airway inflammation via a
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