Ruch R J, Cheng S J, Klaunig J E
Department of Pathology, Medical College of Ohio, Toledo 43699.
Carcinogenesis. 1989 Jun;10(6):1003-8. doi: 10.1093/carcin/10.6.1003.
An antioxidant fraction of Chinese green tea (green tea antioxidant; GTA), containing several catechins, has been previously shown to inhibit 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced tumor promotion in mouse skin. In the present study, GTA was shown to have antioxidative activity toward hydrogen peroxide (H2O2) and the superoxide radical (O2-). GTA also prevented oxygen radical and H2O2-induced cytotoxicity and inhibition of intercellular communication in cultured B6C3F1 mouse hepatocytes and human keratinocytes (NHEK cells). GTA (0.05-50 micrograms/ml) prevented the killing of hepatocytes (measured by lactate dehydrogenase release) by paraquat (1-10 mM) and glucose oxidase (0.8-40 micrograms/ml) in a concentration-dependent fashion. GTA (50 micrograms/ml) also prevented the inhibition of hepatocyte intercellular communication by paraquat (5 mM), glucose oxidase (0.8 micrograms/ml), and phenobarbital (500 micrograms/ml). In addition, GTA (50 micrograms/ml) prevented the inhibition of intercellular communication in human keratinocytes by TPA (100 ng/ml). Cytotoxicity and inhibition of intercellular communication, two possible mechanisms by which tumor promoters may produce their promoting effects were therefore prevented by GTA. The inhibition of these two effects of pro-oxidant compounds may suggest a mechanism by which GTA inhibits tumor promotion in vivo.
中国绿茶的一种抗氧化成分(绿茶抗氧化剂;GTA),含有多种儿茶素,先前已被证明可抑制12 - O - 十四烷酰佛波醇 - 13 - 乙酸酯(TPA)诱导的小鼠皮肤肿瘤促进作用。在本研究中,GTA对过氧化氢(H2O2)和超氧阴离子自由基(O2-)具有抗氧化活性。GTA还可预防氧自由基和H2O2诱导的细胞毒性以及培养的B6C3F1小鼠肝细胞和人角质形成细胞(NHEK细胞)中细胞间通讯的抑制。GTA(0.05 - 50微克/毫升)以浓度依赖的方式预防百草枯(1 - 10毫摩尔)和葡萄糖氧化酶(0.8 - 40微克/毫升)对肝细胞的杀伤作用(通过乳酸脱氢酶释放来测量)。GTA(50微克/毫升)还可预防百草枯(5毫摩尔)、葡萄糖氧化酶(0.8微克/毫升)和苯巴比妥(500微克/毫升)对肝细胞间通讯的抑制作用。此外,GTA(50微克/毫升)可预防TPA(100纳克/毫升)对人角质形成细胞中细胞间通讯的抑制作用。因此,GTA可预防细胞毒性和细胞间通讯的抑制,这是肿瘤促进剂可能产生其促进作用的两种可能机制。对这些促氧化化合物的这两种作用的抑制可能提示了GTA在体内抑制肿瘤促进作用的一种机制。