| Literature DB >> 23792160 |
Bregje van de Wier1, Jiska M Balk, Guido R M M Haenen, Dimosthenis Giamouridis, Jaap A Bakker, Bertine C Bast, Gertjan J M den Hartog, Ger H Koek, Aalt Bast.
Abstract
Plasma citrate levels were found to be elevated in non-alcoholic fatty liver disease (NAFLD) patients. Cellular experiments indicated that increased citrate levels might originate from an excess of fatty acids. The impact of elevated citrate levels on oxidative stress was examined. It was found that citrate stimulated hydrogen peroxide induced intracellular oxidative stress in HepG2 cells. This was related to the promotion of iron mediated hydroxyl radical formation from hydrogen peroxide by citrate. The stimulating effect of citrate on the reactivity of iron promotes oxidative stress, a crucial process in the progression of NAFLD.Entities:
Keywords: ()OH; 2,7-dichlorofluorescin diacetate; 2-deoxy-d-ribose; 5-diethoxyphosphoryl-5-methyl-1-pyrroline N-oxide; Citrate; DCFH-DA; DMPO; DPBS; Deoxyribose; Dulbecco’s phosphate buffered saline; ESR; Fe(2+); FeCl(3); FeSO(4); Fenton reaction; H(2)O(2); HepG2; Hydroxyl radical; Iron; NAFLD; NASH; Non-alcoholic fatty liver disease; Oxidative stress; ROS; electron spin resonance; ferric chloride; ferrous ion; ferrous sulphate; human hepatoma cell line; hydrogen peroxide; hydroxyl radical; non-alcoholic fatty liver disease; non-alcoholic steatohepatitis; reactive oxygen species
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Year: 2013 PMID： 23792160 DOI： 10.1016/j.febslet.2013.06.019
Source DB: PubMed Journal: FEBS Lett ISSN： 0014-5793 Impact factor: 4.124