Green tea polyphenol epigallocatechin-3-gallate protects cells against peroxynitrite-induced cytotoxicity: modulatory effect of cellular G6PD status

Journal of Agricultural and Food Chemistry
Hung-Yao HoDaniel Tsun-Yee Chiu

Abstract

Glucose-6-phosphate dehydrogenase (G6PD) plays important roles in the maintenance of cellular redox balance. It was not until recently that the importance of G6PD in regulation of cellular growth and apoptosis emerged. In the present study, we found that G6PD-deficient fibroblasts were more susceptible to peroxynitrite-induced cytotoxicity. Treatment with peroxynitrite generator 3-morpholinosydnonimine (SIN-1) hydrochloride caused apoptosis in human fibroblast in a dose-dependent manner. This was preceded by a decrease in the intracellular level of glutathione (GSH) as well as accumulation of p53. The extent of apoptosis and glutathione depletion were greater in G6PD-deficient fibroblasts than in the normal counterpart. Pretreatment with green tea polyphenol epigallocatechin-3-gallate (EGCG) effectively blocked peroxynitrite-induced glutathione depletion, p53 accumulation, and apoptosis in both normal and G6PD-deficient cells. EGCG, administered to cells alone or as pretreatment, caused activation of Akt. The protective effect was abolished by phosphatidylinositol 3-kinase (PI3K) inhibitors, wortmannin, and LY294002. Our findings suggest that G6PD deficiency enhances the toxicity of peroxynitrite and that EGCG initiates cell su...Continue Reading

References

Mar 1, 1988·Biochemical Pharmacology·J Robak, R J Gryglewski
Nov 8, 1994·Proceedings of the National Academy of Sciences of the United States of America·W A PryorG L Squadrito
Nov 1, 1996·The American Journal of Physiology·J S Beckman, W H Koppenol
Mar 6, 1997·Biochemical and Biophysical Research Communications·A S PannalaS Singh
Jul 30, 1997·Biochemical and Biophysical Research Communications·G R HaenenA Bast
Jun 2, 1998·FEBS Letters·E A KonorevB Kalyanaraman
Oct 19, 1999·Brain Research. Brain Research Reviews·F TorreillesJ Torreilles
Dec 2, 1999·Genes & Development·S R DattaM E Greenberg
Feb 22, 2001·Free Radical Biology & Medicine·R RadiA Cayota
Sep 4, 2001·Human & Experimental Toxicology·G Aykaç-TokerN Koçak-Toker
Feb 26, 2004·Free Radical Biology & Medicine·Mei-Ling ChengDaniel Tsun-Yee Chiu
Oct 27, 2004·Apoptosis : an International Journal on Programmed Cell Death·M OsakiH Ito

❮ Previous
Next ❯

Citations

Apr 12, 2014·Free Radical Research·H-Y HoD T-Y Chiu
Feb 14, 2013·Fish & Shellfish Immunology·Hangjun ZhangXiuying Jia
May 23, 2008·The Journal of Nutritional Biochemistry·Ana Belén Granado-SerranoSonia Ramos
Nov 30, 2007·Free Radical Biology & Medicine·Tai DuAnthony R White
Aug 30, 2008·The Journal of General Virology·Hung-Yao HoDaniel Tsun-Yee Chiu
Jul 12, 2007·Redox Report : Communications in Free Radical Research·Hung-yao HoDaniel Tsun-yee Chiu
Feb 16, 2013·Food and Chemical Toxicology : an International Journal Published for the British Industrial Biological Research Association·Palaniswamy KalaiselviViswanadha Vijaya Padma
Jul 5, 2007·Journal of Pediatric Hematology/oncology·Farzaneh Foroughinia, Mehran Karimi
Jun 23, 2009·Journal of Agricultural and Food Chemistry·Hung-Yao HoDaniel Tsun-Yee Chiu
Feb 27, 2018·Biomedicine & Pharmacotherapy = Biomédecine & Pharmacothérapie·Muhammad NaveedZhou XiaoHui

❮ Previous
Next ❯

Related Concepts

Related Feeds

AKT Pathway

This feed focuses on the AKT serine/threonine kinase, which is an important signaling pathway involved in processes such as glucose metabolism and cell survival.

Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis