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Biomolecules Nov 2020Diabetic retinopathy (DR) is the leading cause of vision loss among working-age adults. Extensive evidences have documented that oxidative stress mediates a critical... (Review)
Review
Diabetic retinopathy (DR) is the leading cause of vision loss among working-age adults. Extensive evidences have documented that oxidative stress mediates a critical role in the pathogenesis of DR. Acrolein, a product of polyamines oxidation and lipid peroxidation, has been demonstrated to be involved in the pathogenesis of various human diseases. Acrolein's harmful effects are mediated through multiple mechanisms, including DNA damage, inflammation, ROS formation, protein adduction, membrane disruption, endoplasmic reticulum stress, and mitochondrial dysfunction. Recent investigations have reported the involvement of acrolein in the pathogenesis of DR. These studies have shown a detrimental effect of acrolein on the retinal neurovascular unit under diabetic conditions. The current review summarizes the existing literature on the sources of acrolein, the impact of acrolein in the generation of oxidative damage in the diabetic retina, and the mechanisms of acrolein action in the pathogenesis of DR. The possible therapeutic interventions such as the use of polyamine oxidase inhibitors, agents with antioxidant properties, and acrolein scavengers to reduce acrolein toxicity are also discussed.
Topics: Acrolein; Animals; Antioxidants; DNA Damage; Diabetic Retinopathy; Humans; Oxidative Stress; Retina
PubMed: 33233661
DOI: 10.3390/biom10111579 -
Toxicology and Industrial Health Aug 2008Acrolein is a chemical used as an intermediate reactive aldehyde in chemical industry. It is used for synthesis of many organic substances, methionine production, and... (Review)
Review
Acrolein is a chemical used as an intermediate reactive aldehyde in chemical industry. It is used for synthesis of many organic substances, methionine production, and methyl chloride refrigerant. The general population is exposed to acrolein via smoking, second-hand smoke, exposure to wood and plastic smoke. Firefighters and population living or working in areas with heavy automotive traffic may expose to higher level of acrolein via inhalation of smoke or automotive exhaust. Degradation of acrolein in all environmental media occurs rapidly, therefore, environmental accumulation is not expected. Acrolein degrade in 6A days when applied to surface water, and it has not been found as a contaminant in municipal drinking water. Acrolein vapor may cause eye, nasal and respiratory tract irritations in low level exposure. A decrease in breathing rate was reported by volunteers acutely exposed to 0.3A ppm of acrolein. At similar level, mild nasal epithelial dysplasia, necrosis, and focal basal cell metaplasia have been observed in rats. The acrolein effects on gastrointestinal mucosa in the animals include epithelial hyperplasia, ulceration, and hemorrhage. The severity of the effects is dose dependent. Acrolein induces the respiratory, ocular, and gastrointestinal irritations by inducing the release of peptides in nerve terminals innervating these systems. Levels of acrolein between 22 and 249 ppm for 10 min induced a dose-related decrease in substance P (a short-chain polypeptide that functions as a neurotransmitter or neuromodulator).
Topics: Acrolein; Animals; Dose-Response Relationship, Drug; Environmental Pollutants; Humans; Risk Assessment; Toxicity Tests
PubMed: 19028774
DOI: 10.1177/0748233708094188 -
Molecular Nutrition & Food Research Sep 2011
Topics: Acrolein; Animals; Food; Humans
PubMed: 21898907
DOI: 10.1002/mnfr.201190034 -
IARC Monographs on the Evaluation of... 1995
Review
Topics: Acrolein; Animals; Carcinogenicity Tests; Carcinogens; Humans
PubMed: 9097100
DOI: No ID Found -
Environmental Science. Processes &... Nov 2021Acrolein (2-propenal) is a reactive substance undergoing multiple reaction pathways and an airborne pollutant with known corrosive, toxic and hazardous effects to the... (Review)
Review
Acrolein (2-propenal) is a reactive substance undergoing multiple reaction pathways and an airborne pollutant with known corrosive, toxic and hazardous effects to the environment and to human health. So far, investigating the occurrence of acrolein in indoor air has been challenging due to analytical limitations. The classic DNPH-method has proven to be error-prone, even though it is still recommended in specific testing protocols. Thus, different approaches for an accurate determination of ambient acrolein have been introduced. In this work, an overview of already published data regarding emission sources and air concentrations is provided. In addition, a new method for the quantitative determination of acrolein in environmental test chambers and in indoor air is presented. Analysis is carried out using thermal desorption and coupled gas chromatography/mass spectrometry (TD-GC/MS) after sampling on the graphitized carbon black (GCB) Carbograph™ 5TD. All analytical steps have been carefully validated and compared with derivatization techniques (DNPH and DNSH) as well as online detection using PTR-QMS. The sampling time is short due to the low air collection volume of 4 L. Although derivatization is not applied, a detection limit of 0.1 μg m can be achieved. By increasing the sampling volume to 6 L, the limit of detection can be lowered to 0.08 μg m. No breakthrough during sampling or analyte loss during storage of the acrolein laden sampling tubes was found. Therefore, the presented method is robust, easy-to-handle and also very suitable for routine analyses and surveys.
Topics: Acrolein; Atmosphere; Gas Chromatography-Mass Spectrometry; Humans
PubMed: 34591059
DOI: 10.1039/d1em00221j -
Chemical Record (New York, N.Y.) Apr 2021N-alkyl unsaturated imines derived from acrolein, a toxin produced during oxidative stress, and biogenic alkyl amines occur naturally and are considered biologically... (Review)
Review
N-alkyl unsaturated imines derived from acrolein, a toxin produced during oxidative stress, and biogenic alkyl amines occur naturally and are considered biologically relevant compounds. However, despite the recent conceptual and technological advances in organic synthesis, research on the new reactivity of these compounds is lacking. This personal account discusses research on the reactivity that has been overlooked in acrolein imines, including the discovery of new methods to synthesize biologically active compounds, the determination of new functions of relevant imines and their precursors, i. e., aldehydes and amines, and the application of these methods for clinical diagnosis.
Topics: Acrolein; Alzheimer Disease; Breast Neoplasms; Female; Humans; Imines; Molecular Structure; Oxidative Stress
PubMed: 33769681
DOI: 10.1002/tcr.202000146 -
Molecular Nutrition & Food Research Jan 2008Acrolein (2-propenal) is ubiquitously present in (cooked) foods and in the environment. It is formed from carbohydrates, vegetable oils and animal fats, amino acids... (Review)
Review
Acrolein (2-propenal) is ubiquitously present in (cooked) foods and in the environment. It is formed from carbohydrates, vegetable oils and animal fats, amino acids during heating of foods, and by combustion of petroleum fuels and biodiesel. Chemical reactions responsible for release of acrolein include heat-induced dehydration of glycerol, retro-aldol cleavage of dehydrated carbohydrates, lipid peroxidation of polyunsaturated fatty acids, and Strecker degradation of methionine and threonine. Smoking of tobacco products equals or exceeds the total human exposure to acrolein from all other sources. The main endogenous sources of acrolein are myeloperoxidase-mediated degradation of threonine and amine oxidase-mediated degradation of spermine and spermidine, which may constitute a significant source of acrolein in situations of oxidative stress and inflammation. Acrolein is metabolized by conjugation with glutathione and excreted in the urine as mercapturic acid metabolites. Acrolein forms Michael adducts with ascorbic acid in vitro, but the biological relevance of this reaction is not clear. The biological effects of acrolein are a consequence of its reactivity towards biological nucleophiles such as guanine in DNA and cysteine, lysine, histidine, and arginine residues in critical regions of nuclear factors, proteases, and other proteins. Acrolein adduction disrupts the function of these biomacromolecules which may result in mutations, altered gene transcription, and modulation of apoptosis.
Topics: Acrolein; Amino Acids; Ascorbic Acid; Carbohydrates; Cell Death; DNA Adducts; Environmental Exposure; Fatty Acids, Unsaturated; Food; Glutathione; Hot Temperature; Humans; Lipids; Oxidative Stress; Threonine; Nicotiana
PubMed: 18203133
DOI: 10.1002/mnfr.200700412 -
IARC Monographs on the Evaluation of... Feb 1979
Review
Topics: Acrolein; Aldehydes; Animals; Carcinogens; Chemical Phenomena; Chemistry; Cricetinae; Environmental Exposure; Environmental Pollutants; Humans; Industry; Lethal Dose 50; Mice; Mutation; Rabbits; Rats
PubMed: 374236
DOI: No ID Found -
Molecular Nutrition & Food Research Sep 2011Acrolein (Acr) is a ubiquitous environmental contaminant; it also can be generated endogenously by lipid peroxidation. Acr contains a carbonyl group and an olefinic... (Review)
Review
Acrolein (Acr) is a ubiquitous environmental contaminant; it also can be generated endogenously by lipid peroxidation. Acr contains a carbonyl group and an olefinic double bond; it can react with many cellular molecules including amino acids, proteins and nucleic acids. In this review article we focus on updating information regarding: (i) Acr-induced DNA damage and methods of detection, (ii) repair of Acr-DNA damage, (iii) mutagenicity of Acr-DNA adducts, (iv) sequence specificity and methylation effect on Acr-DNA adduct formation and (v) the role of Acr in human cancer. We have found that Acr can inhibit DNA repair and induces mutagenic Acr-dG adducts and that the binding spectrum of Acr in the p53 gene in normal human bronchial epithelial cells is similar to the p53 mutational spectrum in lung cancer. Since Acr-DNA adduct has been identified in human lung tissue and Acr causes bladder cancer in human and rat models, we conclude that Acr is a major lung and bladder carcinogen, and its carcinogenicity arises via induction of DNA damage and inhibition of DNA repair.
Topics: Acrolein; Animals; Carcinogenicity Tests; Carcinogens; DNA Adducts; DNA Damage; DNA Repair; Humans; Lipid Peroxidation; Lung Neoplasms; Mutagenicity Tests; Mutation; Rats; Tumor Suppressor Protein p53; Urinary Bladder Neoplasms
PubMed: 21714128
DOI: 10.1002/mnfr.201100148 -
Molecular Nutrition & Food Research Sep 2011Acrolein is an α,β-unsaturated aldehyde formed by thermal treatment of animal and vegetable fats, carbohydrates and amino acids. In addition it is generated... (Review)
Review
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.
Topics: Acrolein; Administration, Oral; Animals; Carcinogenicity Tests; DNA Adducts; Dogs; Food; Food Analysis; Germany; Humans; Mutagenicity Tests; Rats; Risk Assessment; Solanum tuberosum; Toxicity Tests; Toxicity Tests, Acute; Toxicity Tests, Chronic; Toxicity Tests, Subchronic
PubMed: 21898908
DOI: 10.1002/mnfr.201100481