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Molecules (Basel, Switzerland) Dec 2022We describe the carbonylation of a series of mono and dihydroxy derivatives of polyfluorinated alkylbenzenes and benzocycloalkenes with OH groups at benzylic positions...
We describe the carbonylation of a series of mono and dihydroxy derivatives of polyfluorinated alkylbenzenes and benzocycloalkenes with OH groups at benzylic positions using carbon monoxide in the presence of a superacid (TfOH, a TfOH-SbF mixture, or a FSOH-SbF mixture). It was shown that the superacid-catalyzed addition of CO to various primary and secondary polyfluorinated alcohols and diols gives the corresponding mono- and dicarboxylic acids or lactones. The efficiency of various superacids depending on alcohol structure was evaluated, and FSOH-SbF yielded the best results in most transformations. The addition of CO to secondary 1-arylalkan-1-ols containing vicinal fluorine atoms was found to be accompanied by elimination of HF with the formation of -unsaturated aryl-carboxylic acids. In contrast to primary and secondary alcohols, conversion of tertiary perfluoro-1,1-diarylalkan-1-ols into carbonylation products is not complete, and the resulting carboxylic acids are easily decarboxylated after water treatment of the reaction mixture.
Topics: Molecular Structure; Ethanol; Dicarboxylic Acids; Carbon Monoxide
PubMed: 36557890
DOI: 10.3390/molecules27248757 -
Journal of Hepatology May 2022Hepatitis E virus (HEV) is the most common cause of acute viral hepatitis worldwide and is mainly transmitted via the fecal-oral route or through consumption of...
BACKGROUND & AIMS
Hepatitis E virus (HEV) is the most common cause of acute viral hepatitis worldwide and is mainly transmitted via the fecal-oral route or through consumption of contaminated food products. Due to the lack of efficient cell culture systems for the propagation of HEV, limited data regarding its sensitivity to chemical disinfectants are available. Consequently, preventive and evidence-based hygienic guidelines on HEV disinfection are lacking.
METHODS
We used a robust HEV genotype 3 cell culture model which enables quantification of viral infection of quasi-enveloped and naked HEV particles. For HEV genotype 1 infections, we used the primary isolate Sar55 in a fecal suspension. Standardized quantitative suspension tests using end point dilution and large-volume plating were performed for the determination of virucidal activity of alcohols (1-propanol, 2-propanol, ethanol), WHO disinfectant formulations and 5 different commercial hand disinfectants against HEV. Iodixanol gradients were conducted to elucidate the influence of ethanol on quasi-enveloped viral particles.
RESULTS
Naked and quasi-enveloped HEV was resistant to alcohols as well as alcohol-based formulations recommended by the WHO. Of the tested commercial hand disinfectants only 1 product displayed virucidal activity against HEV. This activity could be linked to phosphoric acid as an essential ingredient. Finally, we observed that ethanol and possibly non-active alcohol-based disinfectants disrupt the quasi-envelope structure of HEV particles, while leaving the highly transmissible and infectious naked virions intact.
CONCLUSIONS
Different alcohols and alcohol-based hand disinfectants were insufficient to eliminate HEV infectivity with the exception of 1 commercial ethanol-based product that included phosphoric acid. These findings have major implications for the development of measures to reduce viral transmission in clinical practice.
LAY SUMMARY
Hepatitis E virus (HEV) showed a high level of resistance to alcohols and alcohol-based hand disinfectants. The addition of phosphoric acid to alcohol was essential for virucidal activity against HEV. This information should be used to guide improved hygiene measures for the prevention of HEV transmission.
Topics: Disinfectants; Ethanol; Hand Sanitizers; Hepatitis E; Hepatitis E virus; Humans
PubMed: 35085595
DOI: 10.1016/j.jhep.2022.01.006 -
International Journal of Molecular... May 2023Alcohol misuse, directly or indirectly as a result of its metabolism, negatively impacts most tissues, including four with critical roles in energy metabolism... (Review)
Review
Alcohol misuse, directly or indirectly as a result of its metabolism, negatively impacts most tissues, including four with critical roles in energy metabolism regulation: the liver, pancreas, adipose, and skeletal muscle. Mitochondria have long been studied for their biosynthetic roles, such as ATP synthesis and initiation of apoptosis. However, current research has provided evidence that mitochondria participate in myriad cellular processes, including immune activation, nutrient sensing in pancreatic β-cells, and skeletal muscle stem and progenitor cell differentiation. The literature indicates that alcohol impairs mitochondrial respiratory capacity, promoting reactive oxygen species (ROS) generation and disrupting mitochondrial dynamics, leading to dysfunctional mitochondria accumulation. As discussed in this review, mitochondrial dyshomeostasis emerges at a nexus between alcohol-disrupted cellular energy metabolism and tissue injury. Here, we highlight this link and focus on alcohol-mediated disruption of immunometabolism, which refers to two distinct, yet interrelated processes. Extrinsic immunometabolism involves processes whereby immune cells and their products influence cellular and/or tissue metabolism. Intrinsic immunometabolism describes immune cell fuel utilization and bioenergetics that affect intracellular processes. Alcohol-induced mitochondrial dysregulation negatively impacts immunometabolism in immune cells, contributing to tissue injury. This review will present the current state of literature, describing alcohol-mediated metabolic and immunometabolic dysregulation from a mitochondrial perspective.
Topics: Humans; Mitochondria; Reactive Oxygen Species; Ethanol; Energy Metabolism; Obesity
PubMed: 37239997
DOI: 10.3390/ijms24108650 -
Cells Dec 2023High levels of alcohol intake alter brain gene expression and can produce long-lasting effects. FK506-binding protein 51 (FKBP51) encoded by is a physical and cellular...
High levels of alcohol intake alter brain gene expression and can produce long-lasting effects. FK506-binding protein 51 (FKBP51) encoded by is a physical and cellular stress response gene and has been associated with alcohol consumption and withdrawal severity. has been previously linked to neurite outgrowth and hippocampal morphology, sex differences in stress response, and epigenetic modification. Presently, primary cultured KO and WT mouse neurons were examined for neurite outgrowth and mitochondrial signal with and without alcohol. We found neurite specification differences between KO and WT; particularly, mesh-like morphology was observed after alcohol treatment and confirmed higher MitoTracker signal in cultured neurons of KO compared to WT at both naive and alcohol-treated conditions. Brain regions that express FKBP51 protein were identified, and hippocampus was confirmed to possess a high level of expression. RNA-seq profiling was performed using the hippocampus of naïve or alcohol-injected (2 mg EtOH/Kg) male and female KO and WT mice. Differentially expressed genes (DEGs) were identified between KO and WT at baseline and following alcohol treatment, with female comparisons possessing a higher number of DEGs than male comparisons. Pathway analysis suggested that genes affecting calcium signaling, lipid metabolism, and axon guidance were differentially expressed at naïve condition between KO and WT. Alcohol treatment significantly affected pathways and enzymes involved in biosynthesis (Keto, serine, and glycine) and signaling (dopamine and insulin receptor), and neuroprotective role. Functions related to cell morphology, cell-to-cell signaling, lipid metabolism, injury response, and post-translational modification were significantly altered due to alcohol. In summary, plays a critical role in the response to acute alcohol treatment by altering metabolism and signaling-related genes.
Topics: Female; Male; Animals; Mice; Ethanol; Lipid Metabolism; Injections; Alcohol Drinking; Glycine; Alcohol-Related Disorders
PubMed: 38201293
DOI: 10.3390/cells13010089 -
Brain and Behavior Jun 2021Embryonic exposure to ethanol leads to a condition of physical, behavioral, and cognitive deficiencies named fetal alcohol spectrum disorders (FASD). The most severe...
INTRODUCTION
Embryonic exposure to ethanol leads to a condition of physical, behavioral, and cognitive deficiencies named fetal alcohol spectrum disorders (FASD). The most severe variations are in fetal alcohol syndrome (FAS), which is easier to diagnose and not studied in animal models. On the other side, the pFAS (partial fetal alcohol syndrome) includes cases of alcohol-related congenital disabilities and neurodevelopmental disorder with an inconclusive diagnosis. In recent years, the zebrafish has become a valuable model to study FASD and its variations.
METHODS
This study characterizes the zebrafish embryonic and larval development after low and moderate ethanol concentration exposure. Fish eggs were exposed to 0.0%, 0.25%, 0.5%, and 1.0% ethanol at 24 hr postfertilization, and embryonic development was observed every 8 hr up to 120 hpf. It evaluated movements, phenotypic abnormalities, hatching, cardiac function and heartbeat frequency, larvae length at 120 hpf, and the apoptotic cells' fluorescence stained with acridine orange.
RESULTS
Embryonic exposure to 0.5% and 1% ethanol presented reduced body size, decreased heartbeat rate, higher numbers of apoptotic cells, and hatching time differences.
CONCLUSIONS
Our results suggest any ethanol exposure during embryogenesis can be harmful and reinforces zebrafish as a suitable model for fetal alcohol spectrum disorders (FASD).
Topics: Animals; Disease Models, Animal; Ethanol; Female; Fetal Alcohol Spectrum Disorders; Larva; Pregnancy; Zebrafish
PubMed: 33939334
DOI: 10.1002/brb3.2062 -
Pharmacology & Therapeutics Aug 2020Alcohol use disorder has multiple characteristics including excessive ethanol consumption, impaired control over drinking behaviors, craving and withdrawal symptoms,... (Review)
Review
Alcohol use disorder has multiple characteristics including excessive ethanol consumption, impaired control over drinking behaviors, craving and withdrawal symptoms, compulsive seeking behaviors, and is considered a chronic condition. Relapse is common. Determining the neurobiological targets of ethanol and the adaptations induced by chronic ethanol exposure is critical to understanding the clinical manifestation of alcohol use disorders, the mechanisms underlying the various features of the disorder, and for informing medication development. In the present review, we discuss ethanol's interactions with a variety of neurotransmitter systems, summarizing findings from preclinical and translational studies to highlight recent progress in the field. We then describe animal models of ethanol self-administration, emphasizing the value, limitations, and validity of commonly used models. Lastly, we summarize the behavioral changes induced by chronic ethanol self-administration, with an emphasis on cue-elicited behavior, the role of ethanol-related memories, and the emergence of habitual ethanol seeking behavior.
Topics: Alcohol Drinking; Animals; Appetite; Behavior, Animal; Dopamine; Ethanol; Humans; Models, Animal; Neuroimmunomodulation; Norepinephrine; Receptors, Opioid; Self Administration
PubMed: 32437827
DOI: 10.1016/j.pharmthera.2020.107573 -
Annals of Agricultural and... Jun 2021According to the World Health Organization (WHO), ethyl alcohol occupies the third place among health risks for the general population, causing damage to health as well... (Review)
Review
According to the World Health Organization (WHO), ethyl alcohol occupies the third place among health risks for the general population, causing damage to health as well as social damage. Ethanol is also considered the greatest risk factor in injuries. Both alcohol and its main metabolite, acetaldehyde, are directly toxic to tissues and lead to several systemic pathologies. Alcohol abuse may also lead to mental health disorders. Although one-in-eight adult Poles abstains from drinking alkohol, 10-20% of adult Poles drink alcohol regularly. It is estimated that this group includes about 900,000 addicts, and over 2,000,000 people who drink alcohol at a risky or harmful level. It affects their occurrence and their consequences Drink- driving is one of the problems most often raised, although alcohol is a documented risk factor in pedestrian accidents. It is also an important risk factor for suicidal behaviour with people under the influence of alcohol choosing more radical and effective methods of committing suicide, such as hanging or 'throwing themselves under a moving vehicle.' Only properly selected and consistently taken preventive actions can improve the tragic statistics related to ethanol stimulating risky and auto-aggressive behaviours. It is also necessary to improve the system for reporting such events because only reliable statistics enable proper assessment of the scale of the problem, and the effectiveness of these activities.
Topics: Accidents, Traffic; Aggression; Alcohol Drinking; Automobile Driving; Ethanol; Humans
PubMed: 34184501
DOI: 10.26444/aaem/118861 -
Microbial Biotechnology Apr 2023Clostridium spp. are suitable for the bioconversion of C -gases (e.g., CO , CO and syngas) into different bioproducts. These products can be used as biofuels and are... (Review)
Review
Clostridium spp. are suitable for the bioconversion of C -gases (e.g., CO , CO and syngas) into different bioproducts. These products can be used as biofuels and are reviewed here, focusing on ethanol, butanol and hexanol, mainly. The production of higher alcohols (e.g., butanol and hexanol) has hardly been reviewed. Parameters affecting the optimization of the bioconversion process and bioreactor performance are addressed as well as the pathways involved in these bioconversions. New aspects, such as mixotrophy and sugar versus gas fermentation, are also reviewed. In addition, Clostridia can also produce higher alcohols from the integration of the Wood-Ljungdahl pathway and the reverse ß-oxidation pathway, which has also not yet been comprehensively reviewed. In the latter process, the acetogen uses the reducing power of CO/syngas to reduce C or C fatty acids, previously produced by a chain elongating microorganism (commonly Clostridium kluyveri), into the corresponding bioalcohol.
Topics: Gases; Biofuels; Fermentation; Ethanol; Butanols; 1-Butanol; Clostridium; Bacteria; Hexanols
PubMed: 36661185
DOI: 10.1111/1751-7915.14220 -
Frontiers in Endocrinology 2023Ganshu Nuodan is a liver-protecting dietary supplement composed of () spore powder, (Lour.) Merr. (), Bunge () and (Fisch.) Bunge. (). However, its pharmacodynamic...
INTRODUCTION
Ganshu Nuodan is a liver-protecting dietary supplement composed of () spore powder, (Lour.) Merr. (), Bunge () and (Fisch.) Bunge. (). However, its pharmacodynamic material basis and mechanism of action remain unknown.
METHODS
A mouse model of acute alcohol liver disease (ALD) induced by intragastric administration of 50% alcohol was used to evaluate the hepatoprotective effect of Ganshu Nuodan. The chemical constituents of Ganshu Nuodan were comprehensively identified by UPLC-QTOF/MS, and then its pharmacodynamic material basis and potential mechanism of action were explored by proteomics and network pharmacology.
RESULTS
Ganshu Nuodan could ameliorate acute ALD, which is mainly manifested in the significant reduction of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in serum and malondialdehyde (MDA) content in liver and the remarkably increase of glutathione (GSH) content and superoxide dismutase (SOD) activity in liver. Totally 76 chemical constituents were identified from Ganshu Nuodan by UPLC-QTOF/MS, including 21 quinones, 18 flavonoids, 11 organic acids, 7 terpenoids, 5 ketones, 4 sterols, 3 coumarins and 7 others. Three key signaling pathways were identified via proteomics studies, namely Arachidonic acid metabolism, Retinol metabolism, and HIF-1 signaling pathway respectively. Combined with network pharmacology and molecular docking, six key targets were subsequently obtained, including Ephx2, Lta4h, Map2k1, Stat3, Mtor and Dgat1. Finally, these six key targets and their related components were verified by molecular docking, which could explain the material basis of the hepatoprotective effect of Ganshu Nuodan.
CONCLUSION
Ganshu Nuodan can protect acute alcohol-induced liver injury in mice by inhibiting oxidative stress, lipid accumulation and apoptosis. Our study provides a scientific basis for the hepatoprotective effect of Ganshu Nuodan in acute ALD mice and supports its traditional application.
Topics: Mice; Animals; Molecular Docking Simulation; Network Pharmacology; Proteomics; Chemical and Drug Induced Liver Injury; Liver Diseases, Alcoholic; Ethanol; Glutathione
PubMed: 37795374
DOI: 10.3389/fendo.2023.1229777 -
Molecules (Basel, Switzerland) Jan 2022The forensic toxicologist is challenged to provide scientific evidence to distinguish the source of ethanol (antemortem ingestion or microbial production) determined in... (Review)
Review
The forensic toxicologist is challenged to provide scientific evidence to distinguish the source of ethanol (antemortem ingestion or microbial production) determined in the postmortem blood and to properly interpret the relevant blood alcohol concentration (BAC) results, in regard to ethanol levels at death and subsequent behavioral impairment of the person at the time of death. Higher alcohols (1-propanol, 1-butanol, isobutanol, 2-methyl-1-butanol (isoamyl-alcohol), and 3-methyl-2-butanol (amyl-alcohol)) are among the volatile compounds that are often detected in postmortem specimens and have been correlated with putrefaction and microbial activity. This brief review investigates the role of the higher alcohols as biomarkers of postmortem, microbial ethanol production, notably, regarding the modeling of postmortem ethanol production. Main conclusions of this contribution are, firstly, that the higher alcohols are qualitative and quantitative indicators of microbial ethanol production, and, secondly that the respective models of microbial ethanol production are tools offering additional data to interpret properly the origin of the ethanol concentrations measured in postmortem cases. More studies are needed to clarify current uncertainties about the origin of higher alcohols in postmortem specimens.
Topics: Alcohols; Autopsy; Blood Alcohol Content; Butanols; Ethanol; Forensic Toxicology; Humans; Pentanols; Postmortem Changes; Propanols
PubMed: 35163964
DOI: 10.3390/molecules27030700