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Heme status affects human hepatic messenger RNA and microRNA expression.
World J Gastroenterol
March 2013
Liver, Digestive and Metabolic Disorders Laboratory, Cannon Research Center, Carolinas Medical Center, 1542 Garden Terrace, Charlotte, NC 28203, USA.
Aim: To assess effects of heme on messenger RNA (mRNA) and microRNA (miRNA) profiles of liver cells derived from humans.
Methods: We exposed human hepatoma cell line Huh-7 cells to excess iron protoporphyrin (heme) (10 μmol/L) or induced heme deficiency by addition of 4, 6-dioxoheptanoic acid (500 μmol/L), a potent inhibitor of aminolevulinic acid dehydratase, for 6 h or 24 h. We harvested total RNA from the cells and performed both mRNA and miRNA array analyses, with use of Affymetrix chips, reagents, and instruments (human genome U133 plus 2.
Lack of hemodynamic effects after extended heme synthesis inhibition by succinylacetone in rats.
J Pharmacol Exp Ther
April 2010
Department of Pharmacology and Toxicology, Queen's University, Kingston, Ontario, Canada.
Hypertyrosinemia (HT) is a life-threatening condition caused in large part by the buildup of tyrosine metabolites and their derivatives. One such metabolite is succinylacetone (SA), a potent irreversible inhibitor of heme biosynthesis. Heme is a key component of numerous enzymes involved in arterial blood pressure (BP) regulation, including nitric-oxide synthase (NOS) and its downstream mediator soluble guanylyl cyclase (sGC).
View Article and Find Full Text PDFSlow-onset inhibition of fumarylacetoacetate hydrolase by phosphinate mimics of the tetrahedral intermediate: kinetics, crystal structure and pharmacokinetics.
Biochem J
March 2007
Arthur F. Scott Laboratory of Chemistry, Reed College, 3203 SE Woodstock Blvd, Portland, OR 97202, USA.
FAH (fumarylacetoacetate hydrolase) catalyses the final step of tyrosine catabolism to produce fumarate and acetoacetate. HT1 (hereditary tyrosinaemia type 1) results from deficiency of this enzyme. Previously, we prepared a partial mimic of the putative tetrahedral intermediate in the reaction catalysed by FAH co-crystallized with the enzyme to reveal details of the mechanism [Bateman, Bhanumoorthy, Witte, McClard, Grompe and Timm (2001) J.
View Article and Find Full Text PDFSynthesis and immunosuppressive activity of novel succinylacetone analogues.
Arch Pharm Res
March 2003
Department of Applied Chemistry, College of Engineering, Chonnam National University, Gwangju 500-757, Korea.
This study describes the synthesis of novel enol esters (3) and triketones (4) as analogues of succinylacetone (SA) (Ed- this abbreviation is introduced here based on your use of it in the body of the paper) and the evaluation on the mouse allogeneic mixed lymphocyte reaction (MLR) and the murine model of antigen-induced paw edema formation for immunosuppressive activity. Enol esters (3a-f) were about 2-4 fold more potent than SA in in vitro activity.
View Article and Find Full Text PDFCYP2E1 overexpression up-regulates both non-specific delta-aminolevulinate synthase and heme oxygenase-1 in the human hepatoma cell line HLE/2E1.
Int J Mol Med
January 2003
Department of Anesthesiology and Resuscitology, Okayama University Medical School, Okayama 700-8558, Japan.
Cytochrome P450 (CYP) is known to turn over rapidly both in vivo in the liver, and in vitro in cultured hepatoma cells expressing CYP. We examined changes in heme metabolism by analyzing gene expression of the non-specific delta-aminolevulinate synthase (ALAS-N), and heme oxygenase-1 (HO-1), the rate limiting enzyme in heme synthesis and catabolism, respectively, in the human hepatoma cell line HLE/2E1, in which CYP2E1 was overexpressed by transfection of its expression vector. Both ALAS-N mRNA and HO-1 mRNA levels were found to be markedly up-regulated in HLE/2E1 cells as compared with those in non-transfected cells (HLE), or in mock-transfected cells (HLE/MOCK).
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