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acetaldehyde/atrofi
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Ethanol and acetaldehyde in imbibing soybean seeds in relation to deterioration.
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Deterioration as evidenced by decline in germination or seedling growth of soybean (cv. Essex) seeds during accelerated aging treatments at 41 C and 100% relative humidity is accompanied by increased levels of acetaldehyde and ethanol in imbibing embryonic axes and seeds. These increases become more
Involvement of acetaldehyde in seed deterioration of some recalcitrant woody species through the acceleration of aerobic respiration.
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The rate of acetaldehyde (Ald) evolution in the deterioration of recalcitrant woody seeds was investigated. Four plant species, Ligustrum japonicum, Quercus serrata, Quercus myrsinaefolia and Camellia japonica, were used for the experiments. Similar to orthodox seeds, all of the recalcitrant seeds
Cytotoxicity of acetaldehyde-derived advanced glycation end-products (AA-AGE) in alcoholic-induced neuronal degeneration.
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BACKGROUND
The Maillard reaction that leads to the formation of advanced glycation end-products (AGEs) plays an important role in the pathogenesis of angiopathy in diabetic patients, in aging and in neurodegenerative processes. We hypothesize that acetaldehyde (AA), one of the main metabolites of
Adrenergic nerve degeneration induced by condensation products of adrenaline and acetaldehyde.
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A PBPK model for evaluating the impact of aldehyde dehydrogenase polymorphisms on comparative rat and human nasal tissue acetaldehyde dosimetry.
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Acetaldehyde is an important intermediate in the chemical synthesis and normal oxidative metabolism of several industrially important compounds, including ethanol, ethyl acetate, and vinyl acetate. Chronic inhalation of acetaldehyde leads to degeneration of the olfactory and respiratory epithelium
Effects on endogenous acetaldehyde production by disulfiram and ethanol feeding on rat pancreas.
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Exogenous acetaldehyde infusion can induce pancreatitis-like injury of the pancreas in some isolated pancreas models, whereas in vivo such treatment has failed to induce pancreatitis. In vivo exogenous acetaldehyde may not be effective because it is rapidly metabolized. The aim of this study was to
Subchronic inhalation of mixtures of cigarette smoke constituents in Xpa-/-p53+/- knock-out mice: a comparison of intermittent with semi-continuous exposure to acetaldehyde, formaldehyde, and acrolein.
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We investigated whether inhaling peak concentrations of aldehydes several times daily is more damaging than semi-continuously inhaling low-dose aldehydes. We exposed Xpa-/-p53+/- knock-out mice either intermittently or semi-continuously to mixed acetaldehyde, formaldehyde, and acrolein. The
Cytoprotective value of lysine, penicillamine, and pyridoxal phosphate against the neurotoxicity of acetaldehyde.
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Rats which received acetaldehyde by intraperitoneal injection on a single occasion sustained neural degeneration in the cerebral cortex detectable with both light and electron microscopy. The degeneration was more intense and included the hippocampus when acetaldehyde exposure was given on 5
Identification of the 37-kd rat liver protein that forms an acetaldehyde adduct in vivo as delta 4-3-ketosteroid 5 beta-reductase.
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Acetaldehyde, the first product of alcohol metabolism, is highly reactive. Several proteins have been shown to be covalently modified by acetaldehyde in vivo. We have previously reported the detection of a cytosolic 37-kd protein-acetaldehyde adduct (-AA) in the liver of alcohol-fed rats. The liver
High-performance liquid chromatographic method for the simultaneous detection of malonaldehyde, acetaldehyde, formaldehyde, acetone and propionaldehyde to monitor the oxidative stress in heart.
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Lipid peroxidation (LPO) is the oxidative deterioration of polyunsaturated fatty acids (PUFA) with the production of lipid hydroperoxides, cyclic peroxides, cyclic endoperoxides, and finally fragmentation to ketones and aldehydes (including malonaldehyde, MDA). Estimation of LPO through MDA
Inhalation toxicity of acetaldehyde in rats. I. Acute and subacute studies.
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The 4-h LC50 of acetaldehyde in rats was determined and found to be 13,300 ppm (24.0 g/m3 air). In a 4-week study groups of 10 male and 10 female rats were exposed to 0, 400, 1000, 2200 or 5000 ppm acetaldehyde for 6 h/day, 5 days/week. Treatment-related changes observed at the 5000 ppm level
Ethanol intake: effect on liver and brain mitochondrial function and acetaldehyde oxidation.
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The effect of a chronic ethanol consumption by forcing rats to drink a 20% v/v ethanol solution as sole drinking fluid, for 3 months, was evaluated on: liver and brain mitochondrial function, the capacity of isolated mitochondria to oxidize acetaldehyde, as well as on the low Km mitochondrial AlDH
[Acetaldehyde adducts in the cerebral cortex of long-term ethanol-fed mice].
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It is assumed that the acetaldehyde binds to the proteins after the consumption of ethanol to form an adduct. Such acetaldehyde adducts are related to organ diseases. We examined 8-week-old female BALB/cAJcl mice which had been on a liquid diet for six months. The alcohol-fed mice's liquid diet
Oxidation of ethanol to acetaldehyde and free radicals by rat testicular microsomes.
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A large number of epidemiological studies evidencing that excessive alcohol consumption is associated with impaired testosterone production and testicular atrophy are available in the literature. One hypothesis to explain the deleterious action of alcohol involves the in situ biotransformation to
Susceptibility to inhalation toxicity of acetaldehyde in Aldh2 knockout mice.
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In this study, we evaluated the inhalation toxicity of acetaldehyde in Aldh2 KO (Aldh -/-) mice, using pathological method. Male C57BL/6 (Aldh2 +/+) mice and Aldh -/- mice were exposed to atmospheres containing acetaldehyde at levels of 0, 125, and 500 ppm for 24 h/day during 14 days. Although the
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