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Presumed phenobarbital-induced Stevens-Johnson syndrome in a 4-year-old female Great Dane.
Vet Q
December 2016
a Department of Medicine and Clinical Biology of Small Animals, Faculty of Veterinary Medicine , Ghent University, Merelbeke , Belgium.
Biochemical characterization of porphobilinogen deaminase-deficient mice during phenobarbital induction of heme synthesis and the effect of enzyme replacement.
Mol Med
January 2005
Porphyria Centre Sweden, Department of Laboratory Medicine, Division of Clinical Chemistry, Karolinska Institute, Karolinska University Hospital, Stockholm, Sweden.
Acute intermittent porphyria (AIP) is a genetic disorder caused by a deficiency of porphobilinogen deaminase (PBGD), the 3rd enzyme in heme synthesis. It is clinically characterized by acute attacks of neuropsychiatric symptoms and biochemically by increased urinary excretion of the porphyrin precursors porphobilinogen (PBG) and 5-aminolevulinic acid (ALA). A mouse model that is partially deficient in PBGD and biochemically mimics AIP after induction of the hepatic ALA synthase by phenobarbital was used in this study to identify the site of formation of the presumably toxic porphyrin precursors and study the effect of enzyme-replacement therapy by using recombinant human PBGD (rhPBGD).
View Article and Find Full Text PDFMolecular mechanism investigation of phenobarbital-induced serum cholesterol elevation in rat livers by microarray analysis.
Arch Toxicol
August 2004
Medicinal Safety Research Labs., Sankyo Co. Ltd., 717 Horikoshi, Fukuroi, 437-0065 Shizuoka, Japan.
Phenobarbital (PB) increases serum total cholesterol levels in rodents and humans. To investigate the underlying molecular mechanisms, we performed a microarray analysis on liver of rats treated repeatedly with 100 mg/kg PB, and examined the serum blood chemistry. The serum concentration of non-esterified fatty acids was decreased from day 1 to day 14 except for day 7, and that of cholesterol was increased from day 4 to day 14.
View Article and Find Full Text PDFEvidence for nitric oxide participation in down-regulation of CYP2B1/2 gene expression at the pretranslational level.
Toxicol Lett
February 1997
The William Harvey Research Institute, St. Bartholomew's Medical College, London, UK.
Septic or inflammatory stimuli suppress drug metabolism by cytochrome P-450 in the liver, presumably at the pretranslational level. We have shown previously that nitric oxide is responsible at least in part for the inhibition by bacterial lipopolysaccharide of phenobarbital-induced CYP2B1/2 activity in vivo. This was attributed to the interaction of nitric oxide with heme in the active-center of cytochrome P450, leading to enzyme inactivation.
View Article and Find Full Text PDFMechanism of protection of lobenzarit against paracetamol-induced toxicity in rat hepatocytes.
Eur J Pharmacol
December 1995
Leiden, Amsterdam Center for Drug Research (LACDR), Department of Pharmacochemistry, Vriji Universiteit, Amsterdam, Netherlands.
The protective effects of lobenzarit, an antioxidative agent and antirheumatic drug, on the cytotoxicity of paracetamol in rat hepatocytes were studied, as well as the inhibitory effects of lobenzarit on cytochrome P-450s and glutathione S-transferases (GSTs) in rat liver. Paracetamol was selected as a model toxin, since it is known to be bioactivated by specific cytochrome P-450s presumably to N-acetyl-p-benzoquinoneimine, a reactive metabolite which upon overdosage of paracetamol causes protein and non-protein thiol depletion, lipid peroxidation and cytotoxicity measurable as LDH leakage. At concentrations of lobenzarit of 0.
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