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Many human pharmaceuticals are weak inhibitors of the cytochrome P450 system in rainbow trout () liver S9 fractions.
Front Toxicol
July 2024
Faculty of Pharmacy, Drug Research Program, University of Helsinki, Helsinki, Finland.
Introduction: Pharmaceutical residues are widely detected in aquatic environment and can be taken up by nontarget species such as fish. The cytochromes P450 (CYP) represent an important detoxification mechanism in fish, like in humans. In the present study, we assessed the correlation of the substrate selectivities of rainbow trout CYP1A and CYP3A homologues with those of human, through determination of the half-maximal inhibitory concentrations (IC) of a total sixteen human pharmaceuticals toward CYP1A-like ethoxyresorufin O-deethylase (EROD) and CYP3A-like 7-benzyloxy-4-trifluoromethylcoumarin O-debenzylase (BFCOD) in rainbow trout () liver S9 fractions (RT-S9).
View Article and Find Full Text PDFNaturalistic comparison of clomethiazole and Diazepam treatment in alcohol withdrawal: effects on oxidative stress, inflammatory cytokines and hepatic biomarkers.
Eur Arch Psychiatry Clin Neurosci
June 2024
Department of Psychiatry, Otto-Von-Guericke-University Magdeburg, Leipziger Str. 44, 39120, Magdeburg, Germany.
Ethanol is metabolized by alcohol dehydrogenase to acetaldehyde and induces cytochrome P450 2E1 (CYP2E1), which generates reactive oxygen species that cause inflammatory liver damage. Clomethiazole, a drug approved for alcohol withdrawal treatment (AWT) in some European countries, inhibits CYP2E1. We hypothesized that clomethiazole would lead to a faster reduction in oxidative stress, inflammatory cytokines, and liver enzymes compared to diazepam treatment.
View Article and Find Full Text PDFEffect of Clomethiazole Vs. Clorazepate on Hepatic Fat and Serum Transaminase Activities in Alcohol-Associated Liver Disease: Results from a Randomized, Controlled Phase II Clinical Trial.
Alcohol Alcohol
March 2023
Centre of Alcohol Research (CAR) University of Heidelberg, Germany, and Department of Medicine, Salem Medical Centre, Heidelberg 69121, Germany.
Aims: Alcohol-associated liver disease (ALD) is a global health problem caused, among other factors, by oxidative stress from the formation of reactive oxygen species (ROS). One important source of ROS is microsomal ethanol metabolism catalyzed by cytochrome P450 2E1 (CYP2E1), which is induced by chronic ethanol consumption. Inhibition of CYP2E1 by clomethiazole (CMZ) decreases oxidative stress in cell cultures and improves ALD in animal studies.
View Article and Find Full Text PDFRole of AMPK-SREBP Signaling in Regulating Fatty Acid Binding-4 (FABP4) Expression following Ethanol Metabolism.
Biology (Basel)
November 2022
Department of Surgery, Atrium Health-Carolinas Medical Center, 1000 Blythe Blvd., Charlotte, NC 28203, USA.
Fatty acid binding protein-4 () is not normally expressed in the liver but is induced in alcohol-dependent liver disease (ALD)). This study sought to identify mechanisms whereby ethanol (EtOH) metabolism alters triglyceride accumulation and production. Human hepatoma cells which were stably transfected to express alcohol dehydrogenase (ADH) or cytochrome P4502E1 (CYP2E1) were exposed to EtOH in the absence/presence of inhibitors of ADH (4-methylpyrazole) or CYP2E1 (chlormethiazole).
View Article and Find Full Text PDFEndoplasmic reticulum-targeted inhibition of CYP2E1 with vitamin E nanoemulsions alleviates hepatocyte oxidative stress and reverses alcoholic liver disease.
Biomaterials
September 2022
College of Pharmaceutical Sciences, Zhejiang University, 866 Yuhangtang Road, Hangzhou, Zhejiang, 310058, PR China. Electronic address:
Alcoholic liver disease (ALD) is a global healthcare problem and socioeconomic issue that is primarily driven by chronic and/or excessive alcohol consumption. Upon alcohol exposure, parenchymal hepatocytes (HCs) up-regulate endoplasmic reticulum (ER)-localized monooxygenase Cytochrome P450 family 2 subfamily E member 1 (CYP2E1) to accelerate the metabolism of ethanol (EtOH), which concurrently exacerbates the production and accumulation of toxic metabolic intermediates, especially reactive oxygen species (ROS), playing a decisive role in the initiation and perpetuation of alcohol-induced liver injury. ALD patients without timely intervention may develop a spectrum of metabolic and functional disorders in the liver, including hepatic steatosis, hepatitis, fibrosis, and even cirrhosis.
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