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Hepatocyte Cytotoxicity Induced by Hydroperoxide (Oxidative Stress Model) or Dicarbonyls (Carbonylation Model): Prevention by Bioactive Nut Extracts or Catechins

Carbonyl and oxidative stress augment the development of diabetic complications. We evaluated the cytoprotectiveness of walnut and hazelnut extracts and catechins for decreasing cytotoxicity, lipid peroxidation, reactive oxygen species (ROS) formation, and protein carbonylation in cell death models of carbonyl and oxidative stress. Polar extracts (methanol or water) showed better cytoprotection than the non-polar (ethyl acetate) nut extracts against hydroperoxide-induced hepatocyte cell death and oxidative stress markers. Catechin flavonoids found in plants, including walnuts and hazelnuts, prevented serum albumin carbonylation in a carbonyl stress model (using glyoxal or methylglyoxal). Hepatocyte protein carbonylation and cell death were prevented and UV spectra data suggested a catechin:methylglyoxal adduct was formed. We conclude that (a) bioactive nut constituents in polar extracts were more protective than non-polar extracts against oxidative stress, and (b) catechins were effective under physiological temperature and pH, at preventing dicarbonyl induced cytotoxicity likely by trapping dicarbonyls or reversing early stage carbonylation.

Identiferoai:union.ndltd.org:TORONTO/oai:tspace.library.utoronto.ca:1807/18164
Date16 December 2009
CreatorsBanach, Monica Sofia
ContributorsO'Brien, Peter J., Jenkins, David J. A.
Source SetsUniversity of Toronto
Languageen_ca
Detected LanguageEnglish
TypeThesis

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