title: Pro-oxidative effects of tea and polyphenols, epigallocatechin-3-gallate and epigallocatechin, on G6PD-deficient erythrocytes in vitro.
abstract: Glucose-6-phosphate dehydrogenase (G6PD)-deficient subjects are vulnerable to chemical-induced hemolysis if exposed to oxidative agents. Recent studies reported that green tea and its constituents might act as pro-oxidants. Our objective was to investigate effects of tea and its polyphenolic components on the oxidative status of human G6PD-deficient erythrocytes. Erythrocytes of G6PD-deficient (n = 8) and normal (n = 8) subjects were incubated with water extracts of 3 types of tea samples (black tea, green tea and decaffeinated green tea extract) and 6 polyphenols. The resulting levels of reduced glutathione (GSH) and glutathione disulphide (GSSG), methemoglobin and plasma hemoglobin were quantified by HPLC and biochemical assays. The tea extracts significantly reduced GSH and increased GSSG levels in G6PD-deficient erythrocytes in a dose-dependent manner (0.5-10 mg/ml), but not in normal erythrocytes. Similar dose-dependent responses to (-)-epigallocatechin (EGC) and (-)-epigallocatechin-3-gallate (EGCG), but not to the other polyphenols, were observed. In G6PD-deficient cells, GSH was reduced by 43.3% (EGC at 0.05 mg/ml) and 33.3% (EGCG at 0.5 mg/ml), compared with pre-challenged levels. The concentration of methemoglobin was increased significantly when challenged with tea extracts, and EGC. Plasma hemoglobin levels were higher in G6PD-deficient samples after exposure to tea extracts, EGCG, EGC and gallic acid, compared with those in normal blood. Tea extracts and polyphenols significantly altered the oxidative status of G6PD-deficient erythrocytes in vitro as demonstrated by the decrease of GSH, and increased GSSG, methemoglobin and plasma hemoglobin. Our data caution against the excessive consumption of concentrated tea polyphenolic products by G6PD-deficient subjects.
authors.affiliation: Institute of Chinese Medicine, The Chinese University of Hong Kong, Hong Kong, SAR, China.
authors.forename: Chun Hay
authors.initials: CH
authors.lastname: Ko
authors.forename: Karen
authors.initials: K
authors.lastname: Li
authors.forename: Pak Cheung
authors.initials: PC
authors.lastname: Ng
authors.forename: Kwok Pui
authors.initials: KP
authors.lastname: Fung
authors.forename: Chung Leung
authors.initials: CL
authors.lastname: Li
authors.forename: Raymond Pui-On
authors.initials: RP
authors.lastname: Wong
authors.forename: Kit Man
authors.initials: KM
authors.lastname: Chui
authors.forename: Goldie Jia-Shi
authors.initials: GJ
authors.lastname: Gu
authors.forename: Edmund
authors.initials: E
authors.lastname: Yung
authors.forename: Chi Chiu
authors.initials: CC
authors.lastname: Wang
authors.forename: Tai Fai
authors.initials: TF
authors.lastname: Fok
mesh_terms: D000328:Adult; D028241:Camellia sinensis / Q000737:chemistry; D002392:Catechin / Q000031:analogs & derivatives* / Q000032:analysis / Q000494:pharmacology; D004912:Erythrocytes / Q000187:drug effects* / Q000201:enzymology; D005419:Flavonoids / Q000032:analysis / Q000494:pharmacology; D005954:Glucosephosphate Dehydrogenase / Q000235:genetics / Q000378:metabolism*; D005955:Glucosephosphate Dehydrogenase Deficiency / Q000235:genetics; D005978:Glutathione / Q000032:analysis; D019803:Glutathione Disulfide / Q000032:analysis; D006801:Humans; D008297:Male; D009154:Mutation; D016877:Oxidants / Q000032:analysis / Q000494:pharmacology*; D010636:Phenols / Q000032:analysis / Q000494:pharmacology; D059808:Polyphenols; D013662:Tea / Q000737:chemistry*
chemical_list: D005419:Flavonoids; D016877:Oxidants; D010636:Phenols; D059808:Polyphenols; D013662:Tea; D002392:Catechin; C045651:epigallocatechin gallate; D005954:Glucosephosphate Dehydrogenase; D005978:Glutathione; C057580:gallocatechol; D019803:Glutathione Disulfide