Central Nervous System Depressants
Toxicity Tests, Acute
National Institute on Alcohol Abuse and Alcoholism (U.S.)
National Institute on Aging (U.S.)
National Institute on Drug Abuse (U.S.)
Ciprofloxacin decreases the rate of ethanol elimination in humans. (1/696)BACKGROUND: Extrahepatic ethanol metabolism is postulated to take place via microbial oxidation in the colon, mediated by aerobic and facultative anaerobic bacteria. AIMS: To evaluate the role of microbial ethanol oxidation in the total elimination rate of ethanol in humans by reducing gut flora with ciprofloxacin. METHODS: Ethanol was administered intravenously at the beginning and end of a one week period to eight male volunteers. Between ethanol doses volunteers received 750 mg ciprofloxacin twice daily. RESULTS: A highly significant (p=0.001) reduction in the ethanol elimination rate (EER) was detected after ciprofloxacin medication. Mean (SEM) EER was 107.0 (5.3) and 96.9 (4.8) mg/kg/h before and after ciprofloxacin, respectively. Faecal Enterobacteriaceae and Enterococcus sp. were totally absent after medication, and faecal acetaldehyde production capacity was significantly (p<0.05) decreased from 0.91 (0.15) to 0.39 (0.08) nmol/min/mg protein. Mean faecal alcohol dehydrogenase (ADH) activity was significantly (p<0. 05) decreased after medication, but ciprofloxacin did not inhibit human hepatic ADH activity in vitro. CONCLUSIONS: Ciprofloxacin treatment decreased the ethanol elimination rate by 9.4%, with a concomitant decrease in intestinal aerobic and facultative anaerobic bacteria, faecal ADH activity, and acetaldehyde production. As ciprofloxacin has no effect on liver blood flow, hepatic ADH activity, or cytochrome CYP2E1 activity, these effects are probably caused by the reduction in intestinal flora. (+info)
Inhibition of advanced glycation endproduct formation by acetaldehyde: role in the cardioprotective effect of ethanol. (2/696)Epidemiological studies suggest that there is a beneficial effect of moderate ethanol consumption on the incidence of cardiovascular disease. Ethanol is metabolized to acetaldehyde, a two-carbon carbonyl compound that can react with nucleophiles to form covalent addition products. We have identified a biochemical modification produced by the reaction of acetaldehyde with protein-bound Amadori products. Amadori products typically arise from the nonenzymatic addition of reducing sugars (such as glucose) to protein amino groups and are the precursors to irreversibly bound, crosslinking moieties called advanced glycation endproducts, or AGEs. AGEs accumulate over time on plasma lipoproteins and vascular wall components and play an important role in the development of diabetes- and age-related cardiovascular disease. The attachment of acetaldehyde to a model Amadori product produces a chemically stabilized complex that cannot rearrange and progress to AGE formation. We tested the role of this reaction in preventing AGE formation in vivo by administering ethanol to diabetic rats, which normally exhibit increased AGE formation and high circulating levels of the hemoglobin Amadori product, HbA1c, and the hemoglobin AGE product, Hb-AGE. In this model study, diabetic rats fed an ethanol diet for 4 weeks showed a 52% decrease in Hb-AGE when compared with diabetic controls (P < 0.001). Circulating levels of HbA1c were unaffected by ethanol, pointing to the specificity of the acetaldehyde reaction for the post-Amadori, advanced glycation process. These data suggest a possible mechanism for the so-called "French paradox," (the cardioprotection conferred by moderate ethanol ingestion) and may offer new strategies for inhibiting advanced glycation. (+info)
Inhibition and stimulation of long-chain fatty acid oxidation by chloroacetaldehyde and methylene blue in rats. (3/696)The effects of chloroacetaldehyde (CAA) and methylene blue, both alone and together, on mitochondrial metabolism, hepatic glutathione content, and bile flow were investigated in rats. Oxidation of [1-14C]palmitic acid, [1-14C]octanoic acid, and [1,4-14C]succinic acid allowed for the differentiation between carnitine-dependent long-chain fatty acid metabolism, medium chain fatty acid oxidation, and citric acid cycle activity, respectively. CAA, a metabolite of the anticancer drug ifosfamide, which may be responsible for ifosfamide-induced encephalopathy, inhibited palmitic acid metabolism but not octanoic or succinic acid oxidation, depleted hepatic glutathione, and stimulated bile flow. Methylene blue, which is clinically used to either prevent or reverse ifosfamide-associated encephalopathy, markedly stimulated palmitic acid oxidation either in the presence or absence of CAA, but did not affect the oxidation of octanoic and succinic acid or hepatic glutathione. Taken together, this study demonstrates that CAA inhibits palmitic acid metabolism. Methylene blue stimulates long-chain fatty acid oxidation, most likely by facilitating the translocation of fatty acids into mitochondria, and compensates for the CAA effect in vivo. (+info)
Mechanisms of protection of catalase by NADPH. Kinetics and stoichiometry. (4/696)NADPH is known to be tightly bound to mammalian catalase and to offset the ability of the substrate of catalase (H2O2) to convert the enzyme to an inactive state (compound II). In the process, the bound NADPH becomes NADP+ and is replaced by another molecule of NADPH. This protection is believed to occur through electron tunneling between NADPH on the surface of the catalase and the heme group within the enzyme. The present study provided additional support for the concept of an intermediate state of catalase, through which NADPH serves to prevent the formation (rather than increase the removal) of compound II. In contrast, the superoxide radical seemed to bypass the intermediate state since NADPH had very little ability to prevent the superoxide radical from converting catalase to compound II. Moreover, the rate of NADPH oxidation was several times the rate of compound II formation (in the absence of NADPH) under a variety of conditions. Very little NADPH oxidation occurred when NADPH was exposed to catalase, H2O2, or the superoxide radical separately. That the ratio exceeds 1 suggests that NADPH may protect catalase from oxidative damage through actions broader than merely preventing the formation of compound II. (+info)
Modification of type III VLDL, their remnants, and VLDL from ApoE-knockout mice by p-hydroxyphenylacetaldehyde, a product of myeloperoxidase activity, causes marked cholesteryl ester accumulation in macrophages. (5/696)Very low density lipoproteins (VLDLs) from apolipoprotein (apo) E2/E2 subjects with type III hyperlipoproteinemia, VLDL remnants, and VLDL from apoE-knockout (EKO) mice are taken up poorly by macrophages. The present study examined whether VLDL modification by the reactive aldehyde p-hydroxyphenylacetaldehyde (pHA) enhances cholesteryl ester (CE) accumulation by J774A.1 macrophages. pHA is the major product derived from the oxidation of L-tyrosine by myeloperoxidase and is a component of human atherosclerotic lesions. Incubation of J774A.1 cells with native type III VLDL, their remnants, and EKO-VLDL increased cellular CE by only 3-, 5-, and 5-fold, respectively, compared with controls. In striking contrast, cells exposed to VLDL modified by purified pHA (pHA-VLDL) exhibited marked increases in cellular CE of 38-, 47-, and 35-fold, respectively (P95%, CE accumulation induced by copper-oxidized VLDL. These results demonstrate a novel mechanism for the conversion of type III VLDLs, their remnants, and EKO-VLDL into atherogenic particles and suggest that macrophage uptake of pHA-VLDL (1) requires catalytically active lipoprotein lipase, (2) involves acyl coenzyme A:cholesterol acyltransferase-mediated cholesterol esterification, and (3) involves pathways distinct from the SR-A. (+info)
Development of a polyclonal antibody with broad epitope specificity for advanced glycation endproducts and localization of these epitopes in Bruch's membrane of the aging eye. (6/696)PURPOSE: To develop an antibody that recognizes a variety of advanced glycation endproduct (AGE) epitopes. METHODS: Glycolaldehyde was used to modify bovine serum albumin and HPLC analysis was used to measure pentosidine formation as an indicator of AGE formation. A polyclonal anti-AGE antibody was synthesized by injecting glycolaldehyde-incubated keyhole limpet hemocyanin into rabbits, affinity purified using AGE modified bovine serum albumin coupled to an affinity resin column, and characterized by immunoblot analysis. RESULTS: HPLC analysis of glycolaldehyde treated bovine serum albumin detected high levels of pentosidine formation, suggesting that glycolaldehyde is a potent precursor for pentosidine. By immunoblot analysis, our antibody recognized carboxymethyllysine and pentosidine, two well-characterized AGEs, as well as other AGE epitopes. Immunohistochemical evaluation showed evidence of AGEs in Bruch's membrane (including basal laminar deposits and drusen), choroidal extracellular matrix, and vessel walls in an 82 year old nondiabetic globe. A similar staining pattern was observed in an age-matched diabetic control. In contrast, no staining was seen with the antibody in a 20 month old nondiabetic globe. CONCLUSIONS: A unique anti-AGE antibody was synthesized that recognizes a variety of AGE epitopes including carboxymethyllysine and pentosidine. Its best use might be in broad surveys of the age-dependent accumulation of a large number of AGE epitopes that might not be revealed by antibodies to pentosidine or CML. (+info)
The effect of inhibition of aldehyde dehydrogenase on nasal uptake of inspired acetaldehyde. (7/696)At exposure concentrations of 750 ppm or more, acetaldehyde is a rodent inhalation carcinogen that induces nasal tumors. Aldehyde dehydrogenase (ALDH) is thought to be an important detoxifying enzyme for aldehydes. Although nasal tissues express ALDH, the importance of this enzyme relative to delivered dosage rates at high-inspired concentrations is not well defined. To provide such information, uptake of inspired acetaldehyde was measured at an inspiratory flow rate that approximated the minute ventilation rate in the surgically isolated nasal cavity of F 344 rats pretreated with either saline (control) or the ALDH inhibitor, cyanamide (10 mg/kg s.c.). ALDH activities (substrate concentration 3 times the K(m)) in anterior (respiratory mucosa) and posterior (olfactory mucosa) nasal tissues averaged 160 and 210 nmol/min), respectively, in control animals (total activity 370 nmol/min), compared to 60 and 80 nmol/min, respectively, in cyanamide-pretreated rats (p < 0.05), indicating that approximately 60% inhibition was obtained. Nasal uptake was measured at 3 inspired concentrations: 10, 300, and 1500 ppm. At these concentrations, acetaldehyde uptake efficiency averaged 54, 37, and 34% in saline-pretreated rats, respectively (p < 0.05). In absolute terms, the delivered dosage rates at these exposure concentrations averaged 21, 420, and 1990 nmol/min. The concentration dependence on uptake suggests a saturable process was involved. At inspired concentrations of 300 ppm or more, the delivered dosage rates exceeded the measured specific activity for nasal ALDH of 370 nmol/min. Cyanamide pretreatment abolished the concentration dependence. Specifically, uptake efficiencies in cyanamide-pretreated rats averaged 30, 27, and 31% at inspired concentrations of 10, 300, and 1500 ppm, respectively (p > 0.05); delivered dosage rates were 12, 310, and 1780 nmol/min. Thus, cyanamide pretreatment reduced nasal-delivered dosage rates at inspired concentrations of 10, 300, and 1500 ppm, respectively by 9, 110, and 210 nmol/min, values that correspond well with the total nasal ALDH activity of 370 nmol/min. In toto, these results suggest that inspired acetaldehyde is metabolized in situ by ALDH, but at exposure concentrations of 300 ppm or greater, the delivered dosage rate may equal or exceed the capacity of this enzyme. (+info)
Kinetics of cytochrome P450 2E1-catalyzed oxidation of ethanol to acetic acid via acetaldehyde. (8/696)The P450 2E1-catalyzed oxidation of ethanol to acetaldehyde is characterized by a kinetic deuterium isotope effect that increases K(m) with no effect on k(cat), and rate-limiting product release has been proposed to account for the lack of an isotope effect on k(cat) (Bell, L. C., and Guengerich, F. P. (1997) J. Biol. Chem. 272, 29643-29651). Acetaldehyde is also a substrate for P450 2E1 oxidation to acetic acid, and k(cat)/K(m) for this reaction is at least 1 order of magnitude greater than that for ethanol oxidation to acetaldehyde. Acetic acid accounts for 90% of the products generated from ethanol in a 10-min reaction, and the contribution of this second oxidation has been overlooked in many previous studies. The noncompetitive intermolecular kinetic hydrogen isotope effects on acetaldehyde oxidation to acetic acid ((H)(k(cat)/K(m))/(D)(k(cat)/K(m)) = 4.5, and (D)k(cat) = 1.5) are comparable with the isotope effects typically observed for ethanol oxidation to acetaldehyde, and k(cat) is similar for both reactions, suggesting a possible common catalytic mechanism. Rapid quench kinetic experiments indicate that acetic acid is formed rapidly from added acetaldehyde (approximately 450 min(-1)) with burst kinetics. Pulse-chase experiments reveal that, at a subsaturating concentration of ethanol, approximately 90% of the acetaldehyde intermediate is directly converted to acetic acid without dissociation from the enzyme active site. Competition experiments suggest that P450 2E1 binds acetic acid and acetaldehyde with relatively high K(d) values, which preclude simple tight binding as an explanation for rate-limiting product release. The existence of a rate-determining step between product formation and release is postulated. Also proposed is a conformational change in P450 2E1 occurring during the course of oxidation and the discrimination of P450 2E1 between acetaldehyde and its hydrated form, the gem-diol. This multistep P450 reaction is characterized by kinetic control of individual reaction steps and by loose binding of all ligands. (+info)
Flushing can also be a side effect of certain medications, such as beta-blockers, aspirin, and some antidepressants. In addition, flushing can be a sign of an underlying condition that affects blood flow or blood vessels, such as Raynaud's disease or lupus.
Treatment for flushing will depend on the underlying cause. For example, if flushing is caused by an allergic reaction, medications such as antihistamines may be prescribed. If the flushing is caused by a medical condition, treatment will focus on managing that condition. In some cases, lifestyle changes such as avoiding triggers, wearing protective clothing, and using cool compresses can help reduce flushing.
It is important to seek medical attention if flushing is severe, persistent, or accompanied by other symptoms such as fever, chest pain, or difficulty breathing. Your healthcare provider can diagnose the underlying cause of flushing and recommend appropriate treatment.
The Diagnostic and Statistical Manual of Mental Disorders, 5th Edition (DSM-5) defines alcohol use disorder as a maladaptive pattern of alcohol use that leads to clinically significant impairment or distress in at least three of the following areas:
1. Drinking more or for longer than intended.
2. Desire or unsuccessful efforts to cut down or control drinking.
3. Spending a lot of time drinking or recovering from its effects.
4. Craving or strong desire to drink.
5. Drinking interferes with work, school, or home responsibilities.
6. Continuing to drink despite social or personal problems caused by alcohol use.
7. Giving up important activities in order to drink.
8. Drinking in hazardous situations (e.g., while driving).
9. Continued drinking despite physical or psychological problems caused or worsened by alcohol use.
10. Developing tolerance (i.e., needing to drink more to achieve the desired effect).
11. Experiencing withdrawal symptoms when alcohol use is stopped or reduced.
The severity of alcoholism is categorized into three subtypes based on the number of criteria met: mild, moderate, and severe. Treatment for alcoholism typically involves a combination of behavioral interventions (e.g., cognitive-behavioral therapy, motivational interviewing) and medications (e.g., disulfiram, naltrexone, acamprosate) to manage withdrawal symptoms and cravings.
In conclusion, alcoholism is a chronic and often progressive disease characterized by excessive and compulsive consumption of alcohol despite negative consequences to physical and mental health, relationships, and social functioning. The diagnostic criteria for alcoholism include a combination of physiological, behavioral, and subjective symptoms, and treatment typically involves a combination of behavioral interventions and medications to manage withdrawal symptoms and cravings.
Vertigo can cause a range of symptoms, including:
* A feeling of spinning or swaying
* Dizziness or lightheadedness
* Blurred vision
* Nausea and vomiting
* Abnormal eye movements
* Unsteadiness or loss of balance
To diagnose vertigo, a healthcare professional will typically conduct a physical examination and ask questions about the patient's symptoms and medical history. They may also perform tests such as the head impulse test or the electronystagmography (ENG) test to assess the function of the inner ear and balance systems.
Treatment for vertigo depends on the underlying cause, but may include medications such as anticholinergics, antihistamines, or benzodiazepines, as well as vestibular rehabilitation therapy (VRT) to help the body adapt to the balance problems. In some cases, surgery may be necessary to treat the underlying cause of vertigo.
In summary, vertigo is a symptom characterized by a false sense of spinning or movement of the surroundings, and can be caused by various conditions affecting the inner ear, brain, or nervous system. Diagnosis and treatment depend on the underlying cause, but may include medications, VRT, and in some cases, surgery.
Acetaldehyde ammonia trimer
Acetaldehyde (data page)
Prokaryotic acetaldehyde dehydrogenase dimerisation domain
Indole-3-acetaldehyde reductase (NADPH)
Indole-3-acetaldehyde reductase (NADH)
Heated tobacco product
Lester O. Krampitz
Aldehyde dehydrogenase (NAD(P)+)
Health effects of tobacco
1988 OSHA PEL Project - Acetaldehyde | NIOSH | CDC
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Greener, cheaper MOF synthesis
- In the current study, we aimed to analyse changes of the ventricular IK1 in the presence of acetaldehyde, the primary metabolite of ethanol. (muni.cz)
- Ethanol is primarily metabolized by alcohol dehydrogenase to acetaldehyde, which is then metabolized by ALDH to acetate and carbon dioxide. (medscape.com)
- Accumulation of acetaldehyde leads to the clinical manifestations of the disulfiram-ethanol interaction. (medscape.com)
- After ingestion of coprine-containing mushrooms, ALDH is irreversibly inhibited and consumption of ethanol results in acetaldehyde accumulation. (medscape.com)
- [ 7 ] Ingestion of ethanol up to 3 days after mushroom ingestion may produce acetaldehyde toxicity. (medscape.com)
- 1. The roles of the hepatocellular redox state and the hepatic acetaldehyde concentration in determining the ethanol elimination rate in fasted rats. (nih.gov)
- 5. Effects of ethanol-derived acetaldehyde on the phosphorylation potential and on the intramitochondrial redox state in intact rat liver. (nih.gov)
- 8. Rate determining factors of ethanol oxidation in hepatocytes from starved and fed rats: effect of acetaldehyde concentration on the rate of NADH oxidation catalyzed by alcohol dehydrogenase. (nih.gov)
- 9. Steady-state metabolism of ethanol in perfused rat livers treated with cyanamide: quantitative analysis of acetaldehyde effects on the metabolic flux rates. (nih.gov)
- 11. Influence of aging on ethanol and acetaldehyde oxidation in female rat liver. (nih.gov)
- 20. Effect of chronic alcohol consumption on ethanol and acetaldehyde metabolism. (nih.gov)
- Exposure to malondialdehyde-acetaldehyde adducts (MAA) and/or citrullinated (CIT) proteins in isolation or in combination significantly influence in vitro inflammatory and fibrotic responses in macrophage and fibroblast cell lines in isolation. (acrabstracts.org)
- Acetaldehyde is a highly reactive compound that causes various forms of damage to DNA , including DNA adducts , single- and/or double-strand breaks (DSBs), point mutations , sister chromatid exchanges (SCEs), and DNA - DNA cross-links. (bvsalud.org)
- Among these, DNA adducts such as N²-ethylidene-2'- deoxyguanosine , N²-ethyl-2'- deoxyguanosine , N²-propano-2'- deoxyguanosine , and N²-etheno-2'- deoxyguanosine are central to acetaldehyde -mediated DNA damage because they are associated with the induction of DNA mutations , DNA - DNA cross-links, DSBs, and SCEs. (bvsalud.org)
- In this article, we review recent advances from studies of acetaldehyde -mediated carcinogenesis in the squamous epithelium , focusing especially on acetaldehyde -mediated DNA adducts . (bvsalud.org)
- We have previously demonstrated that protein adducts formed by the interaction of malondialdehyde (MDA) and acetaldehyde (AA), known as MAA-protein adducts, are present in diseased tissues of individuals with rheumatoid arthritis (RA) or CVD. (nebraska.edu)
- Smith noted that another group had recently independently shown that crossed-aldol reactions of acetaldehyde can be carried out asymmetrically with a proline derivative 2 suggesting that the molecule may be able to participate in numerous organocatalytic processes. (chemistryworld.com)
Hydration of acetylene2
- Results: Acetaldehyde (0.3 - 300 µM) induced a reversible inhibition of IK1 with the concentration causing 50% inhibition (IC50) of 53.7 ± 7.7 µM at -100 mV. (muni.cz)
- In an in vitro reaction setup with NER-proficient and NER-deficient xeroderma pigmentosum group A (XPA) cell extracts, NER reactions were observed in the presence of XPA recombinant proteins in acetaldehyde-treated plasmids. (nih.gov)
- Acetaldehyde is potentially a useful substrate for the Mannich reaction, a carbon-carbon bond-forming process where carbonyl compounds, containing C=O, such as aldehydes, react with compounds containing the C=N bond. (chemistryworld.com)
- The key is simply to add an excess of acetaldehyde to the reaction mixture. (chemistryworld.com)
- But in the presence of an excess of acetaldehyde the imine tends to react with the acetaldehyde rather than with the reaction product. (chemistryworld.com)
- And because this reaction is faster than the polymerisation of the acetaldehyde, we can stop the reaction and extract the product before the polymerisation starts. (chemistryworld.com)
- The reaction is conducted at 90-95 °C, and the acetaldehyde formed is separated from water and mercury and cooled. (procurementresource.com)
- Cardiac inward rectifier potassium current IK1 is inhibited by acetaldehyde at clinically relevant concentrations: a role in arrhythmogenesis related to alcohol consumption? (muni.cz)
- Conclusions: We conclude that the observed changes of IK1 under clinically relevant concentrations of acetaldehyde might contribute to the alcohol-induced alterations of the cardiac electrophysiology, namely in people with a genetic defect of aldehyde dehydrogenase and, thus, higher plasma levels of acetaldehyde who are often native to Asia. (muni.cz)
- Acetaldehyde is produced endogenously by alcohol metabolism and is catalyzed by aldehyde dehydrogenase 2 (ALDH2). (bvsalud.org)
- Alcohol consumption increases blood and salivary acetaldehyde levels, especially in individuals with ALDH2 polymorphisms, which are highly associated with the risk of squamous cell carcinomas in the upper aerodigestive tract. (bvsalud.org)
- To understand hangovers more deeply, take a look at the way our body breaks down alcohol and how a chemical called acetaldehyde is responsible for how you feel after a night of too much drinking. (hangoverkw.com)
- Acetaldehyde (pronounced ass-uh-tal-duh-hyde) is a toxin that your body creates as it tries to break down alcohol. (hangoverkw.com)
- The liver then takes the alcohol and breaks it down into acetaldehyde so that two other enzymes can then turn it into a non-toxic acid similar to vinegar. (hangoverkw.com)
- When someone overindulges in alcohol, which threshold becomes less and less with age, the body is unable to rid itself of all the acetaldehyde it produces. (hangoverkw.com)
- One of the most severe effects of acetaldehyde running rampant through your body is inflammation , which is only made worse by the fact that the alcohol blocks a receptor in your brain that conserves water. (hangoverkw.com)
- In the laboratory, acetaldehyde can also be obtained using as raw materials ethyl alcohol, is the method that many consider almost a sacrilege. (kakprosto.ru)
- This includes investigating roles of various factors such as acetaldehyde, cytochrome P450 2E1 (CYP2E1), vascular endothelial growth factor (VEGF), impaired immune function, and alcohol-induced impaired metabolism of s-adenosylmethionine (SAMe), folate, betaine, iron, and vitamin A. (nih.gov)
- Acetaldehyde can be found in perfumes, dyes, rubber and alcohol, among other products. (yahoo.com)
- Acetaldehyde (other names - ethanal, acetaldehyde) has the chemical formula CH3COH. (kakprosto.ru)
- Acetaldehyde is a colorless liquid with a pungent, fruity odor. (cdc.gov)
- A hangover is a result of the damage which dehydration and acetaldehyde both create. (hangoverkw.com)
- Hangover hospital works at helping overcome the effects of acetaldehyde and dehydration by providing IV saline drips and a mix of antioxidant therapies. (hangoverkw.com)
- Crotonaldehyde is generally produced by aldol condensation of acetaldehyde, followed by dehydration. (cdc.gov)
- U.S. Food and Drug Administration tests have found "unacceptable levels" of some cancer-causing chemicals, including benzene, acetaldehyde and acetal contaminants in some bottles, according to a warning issued Oct. 4. (yahoo.com)
- Acetaldehyde metabolism by wine lactic acid bacteria. (oregonstate.edu)
- 7. Aldehyde dehydrogenase activity as the rate-limiting factor for acetaldehyde metabolism in rat liver. (nih.gov)
- 15. Alteration of acetaldehyde metabolism in carbon tetrachloride-intoxicated rat liver: analysis using liver perfusion system. (nih.gov)
- In non-sensitized GP (n = 8), exposure to acetaldehyde or benzaldehyde did not induce any change in the tested parameters, with the exception of a slight irritation of the respiratory tract as detected by histology and an increased number of alveolar macrophages in animals exposed to acetaldehyde (21.9 +- 1.6 and 42.2 +- 5.4 x 106 cells in control and exposed GP respectively). (archives-ouvertes.fr)
- In sensitized GP, exposure to acetaldehyde induced a moderate irritation of the respiratory tract but no change in biological parameters linked to the inflammatory and allergic responses. (archives-ouvertes.fr)
- However, controlling the stereoselectivity of reactions involving acetaldehyde has proved possible in only a small handful of cases, using expensive and fragile enzymes to catalyse the reactions. (chemistryworld.com)
- Without such measures, acetaldehyde can polymerise, or there can be other unwanted reactions creating by-products that are difficult to separate. (chemistryworld.com)
- In the cell, their reactions with acetaldehyde were studied by using labeled reactants and compared with those with acetone, studied in previous work, which gives a general view of the reactions of ion 1 with carbonyl compounds. (archives-ouvertes.fr)
- 1-142) reveals that, at 200 ppm of acetaldehyde, all exposed persons experienced inflammation of the conjuctivae of the eyes, which manifested as redness. (cdc.gov)
- Acetaldehyde is a volatile flavor compound present in many fermented foods and is important in the production of red and white wines. (oregonstate.edu)
- We also give attention to research on acetaldehyde -mediated DNA repair pathways such as the Fanconi anemia pathway and refer to our studies on the prevention of acetaldehyde -mediated DNA damage . (bvsalud.org)
- ChemSci Pick of the Week (INFOGRAPHIC) -Photodissocation of acetaldehyde occurs via different pathways, including the 'roaming' mechanism. (rsc.org)
- Regulation by acetaldehyde. (nih.gov)
- When the liver creates acetaldehyde, it uses the two other enzymes mentioned above to turn it into a non-toxic acid. (hangoverkw.com)
- What's more, the acetaldehyde continues filtering through the liver until it is all excreted, which puts great strain on the liver to produce more enzymes. (hangoverkw.com)
- A novel two-carbon homologation with N-vinylacetamides and ethyl vinyl ether as acetaldehyde anion equivalents in the synthesis of 9H-xanthene, 9H-thioxanthene, and 9,10-dihydro-9-acridine carboxaldehydes. (novartis.com)
- The 200-ppm 1968 TLV established by the ACGIH for acetaldehyde was based on a sensory irritation study conducted by Silverman, Schulte, and First (1946/Ex. (cdc.gov)
- The ability of malolactic bacteria to degrade free and SO(2)-bound acetaldehyde has implications for sensory and color qualities and the use of SO(2) in wine. (oregonstate.edu)
- Previously, we found that acetaldehyde induces reversible intra-strand GG crosslinks in DNA similar to those induced by cis-diammineplatinum(II) that is subsequently repaired by NER. (nih.gov)
- For other organ failures, there are other antioxidants that can help restore cell function and relieve the damage acetaldehyde creates as it wreaks havoc on the body. (hangoverkw.com)
- Based on extensive epidemiological evidence, the International Agency for Research on Cancer defined acetaldehyde associated with the consumption of alcoholic beverages as a "group 1 carcinogen " (definite carcinogen ) for the esophagus and/or head and neck . (bvsalud.org)
- In particular by reacting acetaldehyde with imines, beta-aminoaldehydes are formed and these can be simply converted into beta-amino acids - many of which could be the basis for new drugs. (chemistryworld.com)
- In this study, we analysed the repairability by NER mechanism and the mutagenesis of acetaldehyde. (nih.gov)
- Trace levels of formaldehyde (50000) and acetaldehyde (75070) were detected in one of the heated hot melt adhesives. (cdc.gov)
- In contrast, acetaldehyde is found to be spread over a region at least 100 times larger in extent. (aanda.org)
- Nine strains of the genera Lactobacillus and Oenococcus were able to metabolize acetaldehyde in a resting cell system, whereas two Pediococcus strains were not. (oregonstate.edu)
- There exists sufficient evidence against acetaldehyde suggesting it to cause a variety of DNA lesions and be carcinogenic to humans. (nih.gov)
- The products contained methanol, benzene and acetaldehyde. (yahoo.com)
- The chemists reacted a range of imines with a large excess of acetaldehyde in the presence of the organocatalyst and discovered to their delight that respectable yields - of around 50 per cent - of the corresponding beta-amino aldehydes were produced in only the desired chiral form. (chemistryworld.com)
- Acetaldehyde" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (rush.edu)
- Details for: Acetaldehyde. (who.int)
- This graph shows the total number of publications written about "Acetaldehyde" by people in this website by year, and whether "Acetaldehyde" was a major or minor topic of these publications. (rush.edu)
- Below are the most recent publications written about "Acetaldehyde" by people in Profiles. (rush.edu)
- Both development and wash-out of the acetaldehyde effect on IK1 showed a single exponential time course with average time constants of 24.5 ± 3.5 s and 41.5 ± 3.6 s at 3 µM, respectively. (muni.cz)
- A coincubation of resting cells of Saccharomyces bayanus Première Cuvée and Oenococcus oeni Lo111 showed that strain Lo111 metabolized acetaldehyde produced by the yeast. (oregonstate.edu)