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. 2006 Feb 15;40(4):570-80.
doi: 10.1016/j.freeradbiomed.2005.09.014. Epub 2005 Nov 9.

Cellular and in vivo hepatotoxicity caused by green tea phenolic acids and catechins

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Cellular and in vivo hepatotoxicity caused by green tea phenolic acids and catechins

Giuseppe Galati et al. Free Radic Biol Med. .

Abstract

Tea phenolic acids and catechins containing gallic acid moieties are most abundant in green tea, and various medical benefits have been proposed from their consumption. In the following, the cytotoxicities of these major tea phenolics toward isolated rat hepatocytes have been ranked and the mechanisms of cytotoxicity evaluated. The order of cytotoxic effectiveness found was epigallocatechin-3-gallate>propyl gallate>epicatechin-3-gallate>gallic acid, epigallocatechin>epicatechin. Using gallic acid as a model tea phenolic and comparing it with the tea catechins and gallic acid-derivative food supplements, the major cytotoxic mechanism found with hepatocytes was mitochondrial membrane potential collapse and ROS formation. Epigallocatechin-3-gallate was also the most effective at collapsing the mitochondrial membrane potential and inducing ROS formation. Liver injury was also observed in vivo when these tea phenolics were administered ip to mice, as plasma alanine aminotransferase levels were significantly increased. In contrast, GSH conjugation, methylation, metabolism by NAD(P)H:quinone oxidoreductase 1, and formation of an iron complex were important in detoxifying the gallic acid. In addition, for the first time, the GSH conjugates of gallic acid and epigallocatechin-3-gallate have been identified using mass spectrometry. These results add insight into the cytotoxic and cytoprotective mechanisms of the simple tea phenolic acids and the more complex tea catechins.

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Comment in

  • A case of hepatotoxicity caused by green tea.
    Federico A, Tiso A, Loguercio C. Federico A, et al. Free Radic Biol Med. 2007 Aug 1;43(3):474. doi: 10.1016/j.freeradbiomed.2007.05.010. Epub 2007 May 16. Free Radic Biol Med. 2007. PMID: 17602963 No abstract available.

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