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Nutrients Sep 2021Approximately 4% of cancers worldwide are caused by alcohol consumption. Drinking alcohol increases the risk of several cancer types, including cancers of the upper... (Review)
Review
Approximately 4% of cancers worldwide are caused by alcohol consumption. Drinking alcohol increases the risk of several cancer types, including cancers of the upper aerodigestive tract, liver, colorectum, and breast. In this review, we summarise the epidemiological evidence on alcohol and cancer risk and the mechanistic evidence of alcohol-mediated carcinogenesis. There are several mechanistic pathways by which the consumption of alcohol, as ethanol, is known to cause cancer, though some are still not fully understood. Ethanol's metabolite acetaldehyde can cause DNA damage and block DNA synthesis and repair, whilst both ethanol and acetaldehyde can disrupt DNA methylation. Ethanol can also induce inflammation and oxidative stress leading to lipid peroxidation and further DNA damage. One-carbon metabolism and folate levels are also impaired by ethanol. Other known mechanisms are discussed. Further understanding of the carcinogenic properties of alcohol and its metabolites will inform future research, but there is already a need for comprehensive alcohol control and cancer prevention strategies to reduce the burden of cancer attributable to alcohol.
Topics: Acetaldehyde; Alcohol Drinking; Alcohol-Induced Disorders; Carcinogenesis; DNA Damage; DNA Methylation; Ethanol; Humans; Neoplasms
PubMed: 34579050
DOI: 10.3390/nu13093173 -
Cellular and Molecular Gastroenterology... 2023Binge drinking in patients with metabolic syndrome accelerates the development of alcohol-associated liver disease. However, the underlying mechanisms remain elusive. We...
BACKGROUND & AIMS
Binge drinking in patients with metabolic syndrome accelerates the development of alcohol-associated liver disease. However, the underlying mechanisms remain elusive. We investigated if oxidative and nonoxidative alcohol metabolism pathways, diet-induced obesity, and adipose tissues influenced the development of acute liver injury in a single ethanol binge model.
METHODS
A single ethanol binge was administered to chow-fed or high-fat diet (HFD)-fed wild-type and genetically modified mice.
RESULTS
Oral administration of a single dose of ethanol induced acute liver injury and hepatic endoplasmic reticulum (ER) stress in chow- or HFD-fed mice. Disruption of the Adh1 gene increased blood ethanol concentration and exacerbated acute ethanol-induced ER stress and liver injury in both chow-fed and HFD-fed mice, while disruption of the Aldh2 gene did not affect such hepatic injury despite high blood acetaldehyde levels. Mechanistic studies showed that alcohol, not acetaldehyde, promoted hepatic ER stress, fatty acid synthesis, and increased adipocyte death and lipolysis, contributing to acute liver injury. Increased serum fatty acid ethyl esters (FAEEs), which are formed by an enzyme-mediated esterification of ethanol with fatty acids, were detected in mice after ethanol gavage, with higher levels in Adh1 knockout mice than in wild-type mice. Deletion of the Ces1d gene in mice markedly reduced the acute ethanol-induced increase of blood FAEE levels with a slight but significant reduction of serum aminotransferase levels.
CONCLUSIONS
Ethanol and its nonoxidative metabolites, FAEEs, not acetaldehyde, promoted acute alcohol-induced liver injury by inducing ER stress, adipocyte death, and lipolysis.
Topics: Animals; Mice; Acetaldehyde; Adipocytes; Esters; Ethanol; Fatty Acids; Lipolysis; Liver; Endoplasmic Reticulum Stress; Chemical and Drug Induced Liver Injury
PubMed: 36243320
DOI: 10.1016/j.jcmgh.2022.10.002 -
International Journal of Environmental... Jan 2023Formaldehyde, a colorless and highly irritating substance, causes cancer of the nasopharynx and leukemia. Furthermore, it is one of the environmental mutagens to which...
INTRODUCTION
Formaldehyde, a colorless and highly irritating substance, causes cancer of the nasopharynx and leukemia. Furthermore, it is one of the environmental mutagens to which humans are most abundantly exposed. Acetaldehyde was recently classified as carcinogen class 1B and mutagen class 2 in Annex VI EC regulation. Occupational exposure to the two aldehydes occurs in a wide variety of occupations and industries. The aim of this study is to deepen exposure to the two aldehydes in the non-traditional productive sectors of bakeries and pastry producers.
METHODS
The evaluation of exposure to formaldehyde and acetaldehyde was conducted in Italy in 2019, in specific tasks and positions of 11 bakeries and pastry producers (115 measures, of which 57.4% were in fixed positions and the rest were personal air sampling). The measurements were performed using Radiello© radial diffusion samplers. A logarithmic transformation of the data was performed, and the correlation between the two substances was calculated. Moreover, linear models considering the log-formaldehyde as the outcome and adjusting for log-acetaldehyde values were used.
RESULTS
The study identified high levels of acetaldehyde and formaldehyde exposure in the monitored workplaces. Higher mean values were observed in the leavening phase (8.39 µg/m and 3.39 µg/m for log-transformed data acetaldehyde and formaldehyde, respectively). The adjusted univariate analyses show statistically significant factors for formaldehyde as the presence of yeast, the presence of type 1 flour, the use of barley, the use of fats, the type of production, the use of spelt, and the presence of type 0 flour.
CONCLUSIONS
The measurements confirmed the release of formaldehyde and acetaldehyde in bakeries and pastry industries, especially in some phases of the work process, such as leavening.
Topics: Humans; Acetaldehyde; Formaldehyde; Occupational Exposure; Aldehydes; Allergens
PubMed: 36767350
DOI: 10.3390/ijerph20031983 -
Applied Microbiology and Biotechnology Dec 20182-Deoxy-D-ribose-5-phosphate aldolase (DERA) is a class I aldolase that offers access to several building blocks for organic synthesis. It catalyzes the stereoselective... (Review)
Review
2-Deoxy-D-ribose-5-phosphate aldolase (DERA) is a class I aldolase that offers access to several building blocks for organic synthesis. It catalyzes the stereoselective C-C bond formation between acetaldehyde and numerous other aldehydes. However, the practical application of DERA as a biocatalyst is limited by its poor tolerance towards industrially relevant concentrations of aldehydes, in particular acetaldehyde. Therefore, the development of proper experimental conditions, including protein engineering and/or immobilization on appropriate supports, is required. The present review is aimed to provide a brief overview of DERA, its history, and progress made in understanding the functioning of the enzyme. Furthermore, the current understanding regarding aldehyde resistance of DERA and the various optimizations carried out to modify this property are discussed.
Topics: Acetaldehyde; Aldehyde-Lyases; Aldehydes; Catalysis; Protein Conformation; Protein Engineering; Ribosemonophosphates; Substrate Specificity
PubMed: 30284013
DOI: 10.1007/s00253-018-9392-8 -
International Journal of Molecular... Sep 2017Acetaldehyde is a highly reactive compound that causes various forms of damage to DNA, including DNA adducts, single- and/or double-strand breaks (DSBs), point... (Review)
Review
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. Among these, DNA adducts such as -ethylidene-2'-deoxyguanosine, -ethyl-2'-deoxyguanosine, -propano-2'-deoxyguanosine, and -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. Acetaldehyde is produced endogenously by alcohol metabolism and is catalyzed by aldehyde dehydrogenase 2 (ALDH2). Alcohol consumption increases blood and salivary acetaldehyde levels, especially in individuals with polymorphisms, which are highly associated with the risk of squamous cell carcinomas in the upper aerodigestive tract. 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. In this article, we review recent advances from studies of acetaldehyde-mediated carcinogenesis in the squamous epithelium, focusing especially on acetaldehyde-mediated DNA adducts. 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.
Topics: Acetaldehyde; Animals; Carcinogenesis; Carcinoma, Squamous Cell; DNA Damage; Esophageal Neoplasms; Ethanol; Head and Neck Neoplasms; Humans
PubMed: 28891965
DOI: 10.3390/ijms18091943 -
Food Chemistry Aug 2023The reactions between malondialdehyde and 2,5-dimethylresorcinol, orcinol, olivetol, and alkylresocinols were studied in an attempt to investigate both if this lipid...
The reactions between malondialdehyde and 2,5-dimethylresorcinol, orcinol, olivetol, and alkylresocinols were studied in an attempt to investigate both if this lipid oxidation product is trapped by phenolics analogously to other reactive carbonyls and to elucidate the chemical structures of the produced adducts. After being formed, malondialdehyde is both partially fractionated to acetaldehyde and oligomerized into dimers and trimers. All these compounds react with phenolics producing three main kinds of derivatives: 5(or 7)-alkyl-7(or 5)-hydroxy-4-methyl-4H-chromene-3-carbaldehydes, 7-alkyl-9-hydroxy-6H-2,6-methanobenzo[d][1,3]dioxocine-5-carbaldehydes, and 4-(3-formylphenyl)-7-hydroxy-4H-chromene-3-carbaldehydes. A total of twenty-four adducts were isolated by semipreparative high-performance liquid chromatography (HPLC) and characterized by mono- and bi-dimensional nuclear magnetic resonance (NMR) spectroscopy and mass spectrometry (MS). Reaction pathways to explain the formation of all these compounds are proposed. Obtained results show that phenolics can trap malondialdehyde producing stable derivatives. The function(s) that such derivatives can play in foods remain(s) to be elucidated.
Topics: Malondialdehyde; Phenols; Acetaldehyde; Food; Magnetic Resonance Spectroscopy
PubMed: 36933433
DOI: 10.1016/j.foodchem.2023.135915 -
Biosensors Nov 2022A new spectroelectrochemical two-enzyme sensor system has been developed for the detection of acetaldehyde in wine. A combination of spectroscopy and electrochemistry...
A new spectroelectrochemical two-enzyme sensor system has been developed for the detection of acetaldehyde in wine. A combination of spectroscopy and electrochemistry improves the analytical features of the electrochemical sensor because the optical information collected with this system is only associated with acetaldehyde and avoids the interferents also present in wines as polyphenols. Spectroelectrochemical detection is achieved by the analysis of the optical properties of the K[Fe(CN)]/K[Fe(CN)] redox couple involved in the enzymatic process: aldehyde dehydrogenase catalyzes the aldehyde oxidation using β-nicotinamide adenine dinucleotide hydrate (NAD) as a cofactor and, simultaneously, diaphorase reoxidizes the NADH formed in the first enzymatic process due to the presence of K[Fe(CN)]. An analysis of the characteristic UV-vis bands of K[Fe(CN)] at 310 and 420 nm allows the detection of acetaldehyde, since absorption bands are only related to the oxidation of this substrate, and avoids the contribution of other interferents.
Topics: Acetaldehyde; Wine; NAD; Electrochemistry; Oxidation-Reduction
PubMed: 36421150
DOI: 10.3390/bios12111032 -
Environmental Pollution (Barking, Essex... Nov 2018This study reports a spatiotemporal characterization of formaldehyde and acetaldehyde in the summer and winter of 2017 in the urban area of Shiraz, Iran. Sampling was...
This study reports a spatiotemporal characterization of formaldehyde and acetaldehyde in the summer and winter of 2017 in the urban area of Shiraz, Iran. Sampling was fulfilled according to EPA Method TO-11 A. The inverse distance weighting (IDW) procedure was used for spatial mapping. Monte Carlo simulations were conducted to evaluate carcinogenic and non-cancer risk owing to formaldehyde and acetaldehyde exposure in 11 age groups. The average concentrations of formaldehyde/acetaldehyde in the summer and winter were 15.07/8.40 μg m and 8.57/3.52 μg m, respectively. The formaldehyde to acetaldehyde ratios in the summer and winter were 1.80 and 2.43, respectively. The main sources of formaldehyde and acetaldehyde were photochemical generation, vehicular traffic, and biogenic emissions (e.g., coniferous and deciduous trees). The mean inhalation lifetime cancer risk (LTCR) values according to the Integrated Risk Information System (IRIS) for formaldehyde and acetaldehyde in summer and winter ranged between 7.55 × 10 and 9.25 × 10, which exceed the recommended value by US EPA. The average LTCR according to the Office of Environmental Health Hazard Assessment (OEHHA) for formaldehyde and acetaldehyde in summer and winter were between 4.82 × 10 and 2.58 × 10, which exceeds recommended values for five different age groups (Birth to <1, 1 to <2, 2 to <3, 3 to <6, and 6 to <11 years). Hazard quotients (HQs) of formaldehyde ranged between 0.04 and 4.18 for both seasons, while the HQs for acetaldehyde were limited between 0.42 and 0.97.
Topics: Acetaldehyde; Air Pollutants; Carcinogens; Environmental Exposure; Environmental Monitoring; Formaldehyde; Humans; Iran; Seasons
PubMed: 30373039
DOI: 10.1016/j.envpol.2018.07.037 -
International Journal of Environmental... Apr 2010Alcohol abuse is a serious medical and social problem. Although light to moderate alcohol consumption is beneficial to cardiovascular health, heavy drinking often... (Review)
Review
Alcohol abuse is a serious medical and social problem. Although light to moderate alcohol consumption is beneficial to cardiovascular health, heavy drinking often results in organ damage and social problems. In addition, genetic susceptibility to the effect of alcohol on cancer and coronary heart disease differs across the population. A number of mechanisms including direct the toxicity of ethanol, its metabolites [e.g., acetaldehyde and fatty acid ethyl esters (FAEEs)] and oxidative stress may mediate alcoholic complications. Acetaldehyde, the primary metabolic product of ethanol, is an important candidate toxin in developing alcoholic diseases. Meanwhile, free radicals produced during ethanol metabolism and FAEEs are also important triggers for alcoholic damages.
Topics: Acetaldehyde; Alcoholism; Ethanol; Humans; Oxidative Stress; Polymorphism, Genetic
PubMed: 20617031
DOI: 10.3390/ijerph7041285 -
IARC Monographs on the Evaluation of... 1999
Review
Topics: Acetaldehyde; Animals; Carcinogenicity Tests; Carcinogens; Humans; Mutagenicity Tests; Mutagens; Neoplasms; Neoplasms, Experimental; Occupational Exposure
PubMed: 10476449
DOI: No ID Found