After long-term exhibition to halothane (up to 96 hours), centrolobular hepatic damage (fatty degeneration, necrobiosis and necrosis) developed in rats, proportionally to the number of anesthesias and shortening of the intervals. From these results no hepatotoxic effect of halothane can be derived, since the alterations might be caused by hypoxia alone.
Download full-text PDF |
Source |
|---|
Publication Analysis
Top Keywords
Similar Publications
Molecular mechanisms underlying hepatoprotective activity of lutein in the context of intestinal failure-associated liver disease.
Pharmacol Res
November 2024
Department of Pharmaceutical Chemistry, Poznan University of Medical Sciences, Rokietnicka 3, Poznan 60-806, Poland. Electronic address:
Intestinal failure-associated liver disease (IFALD) is a spectrum of liver diseases occurring in patients not exposed to liver-damaging factors other than those linked to intestinal dysfunction. The pathogenesis of this disease is multifactorial. It is estimated that up to 90 % of people taking long-term parenteral nutrition may develop IFALD, with particular risk for premature neonates and infants due to their immature antioxidant protection and bile acid metabolism.
View Article and Find Full Text PDFIn silico profiling of nonsynonymous SNPs of fat mass and obesity-associated gene: possible impacts on the treatment of non-alcoholic fatty liver disease.
Lipids Health Dis
January 2023
Department of Nutrition, Institute of Basic Medical Sciences, Faculty of Medicine, University of Oslo, Oslo, Norway.
Background: Nonalcoholic fatty liver, or NAFLD, is the most common chronic liver ailment. It is characterized by excessive fat deposition in hepatocytes of individuals who consume little or no alcohol and are unaffected by specific liver damaging factors. It is also associated with extrahepatic manifestations such as chronic kidney disease, cardiovascular disease, and sleep apnea.
View Article and Find Full Text PDFTGF-beta enhances alcohol dependent hepatocyte damage via down-regulation of alcohol dehydrogenase I.
J Hepatol
March 2010
Molecular Hepatology-Alcohol Dependent Diseases, II. Medical Clinic, Faculty of Medicine at Mannheim, University of Heidelberg, Theodor-Kutzer-Ufer 1-3, Mannheim, Germany.
Background & Aims: Adverse alcohol effects in the liver involve oxidative metabolism, fat deposition and release of fibrogenic mediators, including TGF-beta. The work presents an assessment of liver damaging cross-talk between ethanol and TGF-beta in hepatocytes.
Methods: To investigate TGF-beta effects on hepatocytes, microarray analyses were performed and validated by qRT-PCR, Western blot analysis and immunohistochemistry.
The influence of the free radical scavenger 2,4-tetra-O-methyl-furfurylidene-sorbitol (MSF) on the carrageenan-induced hind-paw inflammation in rats as well as its influence on the anti-inflammatory and toxic activities of indomethacin is evaluated in comparison with thiola, thioctic acid, silymarin, reduced glutathione and propylgallate. MSF has been previously shown to prevent, in rats, the liver damaging effects of CCl4, ethionine, allylic alcohol and amanita phalloides row extracts. MSF, but not the other scavengers, exhibits moderate anti-inflammatory properties and markedly potentiates the anti-inflammatory activity indomethacin.
View Article and Find Full Text PDFAt present no sufficiently sensitive liver function tests are available to exactly detect small liver impairments caused by drugs. In this respect immunological quantitation of serum proteins could be useful. We have determined quantitative alterations of four serum proteins (IgG, transferrin, alpha 2-AP = alpha 2-acute phase protein, VLDL = very low density lipoprotein) from rats treated with aminophenazone, phenazone and propyphenazone (each 1,55 mmol/kg body mass/d).
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!