Inhibition of aflatoxin B1-induced initiation of hepatocarcinogenesis in the rat by green tea

Qin, Guozhong; Gopalan-Kriczky, Prathima; Su, Jianjia; Ning, Yaoyu; Lotlikar, Prabhakar D.

doi:10.1016/s0304-3835(96)04568-5

Cited by 60 publications

(22 citation statements)

References 19 publications

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“…Many studies have demonstrated that green tea polyphenols (GTP) inhibit various chemically induced cancers in experimental animals and epidemiological studies also point to the potential benefit of these compounds (54,91). Qin et al (61) studied the effects of GTP in drinking water for two or four weeks to protect against the development of AFB 1 -induced hepatocarcinogenesis in the rat. Data from this investigation revealed that AFB 1 -DNA binding in the liver was significantly inhibited by ∼20%-30% in animals pretreated with green tea and that the burden of preneoplastic lesions was significantly inhibited by 60%-70%.…”

Section: Secondary Preventionmentioning

confidence: 99%

Protective Interventions to Prevent Aflatoxin-Induced Carcinogenesis in Developing Countries

Groopman

Kensler

Wild

2008

Annu. Rev. Public Health

255

163

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The public health impact of aflatoxin exposure is pervasive in economically developing countries; consequently, we need to design intervention strategies for prevention that are practicable for these high-risk populations. The adverse health consequences of aflatoxins in populations are quite varied, eliciting acute effects, such as rapid death, and chronic outcomes, such as hepatocellular carcinoma. Furthermore, a number of epidemiological studies describe a variety of general adverse health effects associated with aflatoxin, such as impaired growth in children. Thus, the magnitude of the problem is disseminated across the entire spectrum of age, gender, and health status in the population. The aflatoxins multiplicatively increase the risk of liver cancer in people chronically infected with hepatitis B virus (HBV), which illustrates the deleterious impact that even low toxin levels in the diet can pose for human health. Thus other aflatoxin interactions, which likely contribute to the diesease burden, still remain to be identified. Therefore, many diverse and appropriate strategies for disease prevention are needed to decrease the incidence of aflatoxin carcinogenesis in developing countries.

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Section: Secondary Preventionmentioning

confidence: 99%

Protective Interventions to Prevent Aflatoxin-Induced Carcinogenesis in Developing Countries

Groopman

Kensler

Wild

2008

Annu. Rev. Public Health

255

163

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“…Similarly, AFQ 1 formation is mediated via CYP3A2 and CYP2B (Eaton and Gallagher, 1994;Buetler et al, 1996). Furthermore, Qin et al (1997) have reported that the pretreatment of rats with 0.5 green tea in their drinking water for 2 or 4 weeks did not produce a significant increase in cytochrome P450 content but enhanced microsome-mediated formation of non-toxic hydroxylated metabolites of AFB 1 by 2 3 fold. These reports support our explanation.…”

Section: Discussionmentioning

confidence: 99%

Suppressive effect of (-)-epigallocatechin gallate on 7,12-dimethylbenz[a]anthracene-induced chromosome aberrations in rat bone marrow cells

Ito¹

2005

Environ. Mutagen Res.

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The suppressive effect of (-)-epigallocatechin gallate (EGCG), the major polyphenolic constituent present in green tea, on 7,12-dimethylbenz [a]anthracene (DMBA)-induced chromosome aberrations (CA) in rat bone marrow cells was studied. Rats given EGCG before the DMBA injection displayed a considerably suppressed frequency of DMBA-induced CA in their bone marrow cells. The suppressive effect of EGCG (60 mg/kg body weight) given 24 h before was observed 24, 30, 48 and 72 h after the DMBA injection, but not at the early period (6, 12 and 18 h) after the DMBA treatment. On the other hand, EGCG (60 mg/kg body weight) given 0.5 h before DMBA suppressed DMBA-induced CA at all periods after the DMBA injection. The suppression of EGCG given 24 h or 0.5 h before was observed for all doses of DMBA (25, 50, 75 and 100 mg/kg) investigated. EGCG given at 60 mg/kg body weight 0.5 h before the DMBA injection showed greater suppressive effect than the same dose given 24 h before. The suppressive effect of EGCG given 0.5 h before was dosedependent in the range of 20 60 mg/kg body weight. Methyl methanesulfonate (MMS: direct-acting carcinogen)-induced CA were not suppressed by EGCG.The administration of dehydroepiandrosterone (DHEA), a typical substrate for hydroxysteroid sulfotransferases, 0.5 h before DMBA injection also significantly suppressed DMBA-induced CA but DHEA given 24 h before did not.These results suggest that EGCG has two different suppression mechanisms for DMBA-induced CA depending on the administration time. The suppression of DMBA-induced CA by EGCG given 24 h or 0.5 h before may result from the modification of microsomal enzyme system or the inhibition of sulfotransferase activity by EGCG, respectively. We have previously reported (Ito et al., 1989) that the administration of GTE or GTP mixture before aflatoxin B 1 (AFB 1 ) injection in rats significantly suppressed AFB 1 -induced chromosome aberrations (CA) in bone marrow cells. Furthermore, we have reported (Ito and Ito, 2001) the suppressive effect of EGCG on AFB 1 -induced CA in rat bone marrow cells. EGCG given 24 h before the AFB 1 injection suppressed AFB 1 -induced CA but not when given 2 h before; the same was true for GTE or GTP mixture. This suppression seems to be due to modification of the microsomal enzyme system by EGCG.In this study, we investigated the suppressive effect of EGCG on CA induced by 7,12-dimethylbenz[a]anthracene (DMBA: indirect-acting carcinogen, as is AFB 1 ) and by methyl methanesulfonate (MMS: direct-acting carcinogen, needs no metabolic activation). Materials and Methods ChemicalsEGCG was purchased from Kurita Kogyo Co. (Tokyo, Japan). DMBA, dehydroepiandrosterone (DHEA) and colchicine were obtained from Wako Pure Chemicals Co. (Tokyo, Japan), MMS was from Aldrich (Milwaukee, WI), and dimethyl fulfoxide (DMSO: spectrophotometric grade) was from E. Merck A.G., (Darmstadt, F.R.G.). Animal experimentsMale rats of the Wistar strain (Charles River Japan, Inc., Kanagawa, Japan), aged 28 35 days and weighing 80 110 g, were used. Each...

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“…This suggestion is supported by the following reports. Qin et al 46) have reported that the pretreatment of rats with 0.5% green tea in their drinking water for 2 or 4 weeks did not produce a significant increase in cytochrome P450 content but enhanced microsome-mediated formation of non-toxic hydroxylated metabolites of AFB 1 by 2-3 fold. It has also been reported by Sohn et al 47) and Bu-Abbas et al 48) that rats administered GTE for 4 or 6 weeks displayed no significant increase in total cytochrome P450 content in the liver but did display a significant increase in O-dealkylase activity of ethoxyresorufin (CYP1A1), methoxyresorufin (CYP1A2) and pentoxyresorufin (CYP2B1).…”

Section: Discussionmentioning

confidence: 99%

Suppressive Effect of (-)-Epigallocatechin Gallate on Aflatoxin B1-induced Chromosome Aberrations in Rat Bone Marrow Cells.

Ito¹,

Itô²

2001

JOURNAL OF HEALTH SCIENCE

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The suppressive effect of (-)-epigallocatechin gallate (EGCG), the major polyphenolic constituent present in green tea, on aflatoxin B 1 (AFB 1 )-induced chromosome aberrations (CA) in rat bone marrow cells was studied. The administration of EGCG 24 hr before the AFB 1 injection significantly suppressed AFB 1 -induced CA. The suppression was observed 18 hr, 24 hr and 48 hr after the AFB 1 treatment but no suppressive effect was observed at the early period (6 hr and 12 hr) after the AFB 1 treatment. Furthermore, the suppression was observed in all doses of AFB 1 (1, 5, 10 and 20 mg/kg) investigated. Rats given EGCG 2 hr before the AFB 1 injection displayed no suppressive effect. The suppressive effect of EGCG paralleled the dose of EGCG when given in a dose range of 10-60 mg/kg body weight. The administration of (-)-epicatechin gallate 24 hr before the AFB 1 injection significantly suppressed AFB 1 -induced CA as well as EGCG. On the other hand, in rats given green tea polyphenols (GTP) 2 hr before the AFB 1 injection, (-)-epigallocatechin and gallic acid significantly suppressed AFB 1 -induced CA. The pretreatment with EGCG or gallic acid did not induce the drug-metabolizing enzymes in rat liver, such as cytochrome P450 and glutathione S-transeferase. Rats given 2% green tea infusion as the sole source of drinking water for four days before sacrifice displayed significantly suppressed AFB 1 -induced CA. However, rats given various kinds of canned tea for four days showed no suppressive effect. The amount of GTP in canned tea determined by high performance liquid chromatography (HPLC) analysis was much less than that in 2% green tea infusion.

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Inhibition of aflatoxin B1-induced initiation of hepatocarcinogenesis in the rat by green tea

Cited by 60 publications

References 19 publications

Protective Interventions to Prevent Aflatoxin-Induced Carcinogenesis in Developing Countries

Protective Interventions to Prevent Aflatoxin-Induced Carcinogenesis in Developing Countries

Suppressive effect of (-)-epigallocatechin gallate on 7,12-dimethylbenz[a]anthracene-induced chromosome aberrations in rat bone marrow cells

Suppressive Effect of (-)-Epigallocatechin Gallate on Aflatoxin B1-induced Chromosome Aberrations in Rat Bone Marrow Cells.

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