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Please use this identifier to cite or link to this item: http://hdl.handle.net/1807/24568

Title: Hepatocyte Molecular Cytotoxic Mechanism Study of Fructose and its Metabolites Involved in Nonalcoholic Steatohepatitis and Hyperoxaluria
Authors: Feng, Yan
Advisor: O'Brien, Peter J.
Department: Pharmaceutical Sciences
Keywords: Fructose
Hepatocyte toxicity
Nonalcoholic Steatohepatitis
Hyperoxaluria
Issue Date: 26-Jul-2010
Abstract: High chronic fructose consumption is linked to a nonalcoholic steatohepatitis (NASH) type of hepatotoxicity. Oxalate is the major endpoint of fructose metabolism, which accumulates in the kidney causing renal stone disease. Both diseases are life-threatening if not treated. Our objective was to study the molecular cytotoxicity mechanisms of fructose and some of its metabolites in the liver. Fructose metabolites were incubated with primary rat hepatocytes, but cytotoxicity only occurred if the hepatocytes were exposed to non-toxic amounts of hydrogen peroxide such as those released by activated immune cells. Glyoxal was most likely the endogenous toxin responsible for fructose induced toxicity formed via autoxidation of the fructose metabolite glycolaldehyde catalyzed by superoxide radicals, or oxidation by Fenton’s hydroxyl radicals. As for hyperoxaluria, glyoxylate was more cytotoxic than oxalate presumably because of the formation of condensation product oxalomalate causing mitochondrial toxicity and oxidative stress. Oxalate toxicity likely involved pro-oxidant iron complex formation.
URI: http://hdl.handle.net/1807/24568
Appears in Collections:Master
Leslie L. Dan Faculty of Pharmacy - Master theses

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