Get 20M+ Full-Text Papers For Less Than $1.50/day. Start a 14-Day Trial for You or Your Team.

Learn More →

MOLECULAR EPIDEMIOLOGY AND CANCER PREVENTION: Protection by green tea, black tea, and indole-3-carbinol against 2-amino-3-methylimidazo[4,5- ...

MOLECULAR EPIDEMIOLOGY AND CANCER PREVENTION: Protection by green tea, black tea, and... Male F344 rats were exposed for 8 weeks to extracts of green tea (2% w/v) or black tea (1% w/v), or to 0.1% dietary indole-3-carbinol (I3C). In weeks 3 and 4 of the study, rats were given 2-amino-3-methylimidazo[4, 5-f]-quinoline (IQ) every other day by oral gavage (50 mg/kg body wt) in order to induce aberrant crypt foci (ACF) in the colon. Compared with controls given IQ alone, all three inhibitors reduced the number of total aberrant crypts per colon, and green tea and I3C inhibited significantly the mean number of ACF (P< 0.05). Rats pre-treated with green tea, black tea, or I3C and given a single p.o. injection of 50 mg IQ/kg body wt 24–48 h before sacrifice had reduced levels of IQ-DNA adducts in the liver, and excreted lower amounts of IQ and other promutagens in the urine and feces. Inhibitors also reduced the excretion of IQ-sulfamate in the urine, but increased the relative amounts of IQ-5-O-sulfate and IQ-5-O-glucuronide. Western blotting together with assays for 7-ethoxyresorufin O-deethylase and methoxyresorufin O-demethylase established that I3C preferentially induced cytochrome P4501A1 over 1A2, consistent with the altered profile of urinary metabolites. However, both teas caused slight induction of cytochrome P4501A2 versus 1A1, which would be predicted to enhance the activation of IQ. Thus, green tea and black tea are likely to protect against IQ-DNA adducts and ACF by mechanisms other than induction of cytochromes P450, such as inhibition of enzymes which activate IQ or the scavenging of reactive intermediates. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Carcinogenesis Oxford University Press

MOLECULAR EPIDEMIOLOGY AND CANCER PREVENTION: Protection by green tea, black tea, and indole-3-carbinol against 2-amino-3-methylimidazo[4,5- ...

Loading next page...
 
/lp/oxford-university-press/molecular-epidemiology-and-cancer-prevention-protection-by-green-tea-dzIvGQyc26

References (16)

Publisher
Oxford University Press
Copyright
© Oxford University Press
ISSN
0143-3334
eISSN
1460-2180
DOI
10.1093/carcin/17.7.1429
Publisher site
See Article on Publisher Site

Abstract

Male F344 rats were exposed for 8 weeks to extracts of green tea (2% w/v) or black tea (1% w/v), or to 0.1% dietary indole-3-carbinol (I3C). In weeks 3 and 4 of the study, rats were given 2-amino-3-methylimidazo[4, 5-f]-quinoline (IQ) every other day by oral gavage (50 mg/kg body wt) in order to induce aberrant crypt foci (ACF) in the colon. Compared with controls given IQ alone, all three inhibitors reduced the number of total aberrant crypts per colon, and green tea and I3C inhibited significantly the mean number of ACF (P< 0.05). Rats pre-treated with green tea, black tea, or I3C and given a single p.o. injection of 50 mg IQ/kg body wt 24–48 h before sacrifice had reduced levels of IQ-DNA adducts in the liver, and excreted lower amounts of IQ and other promutagens in the urine and feces. Inhibitors also reduced the excretion of IQ-sulfamate in the urine, but increased the relative amounts of IQ-5-O-sulfate and IQ-5-O-glucuronide. Western blotting together with assays for 7-ethoxyresorufin O-deethylase and methoxyresorufin O-demethylase established that I3C preferentially induced cytochrome P4501A1 over 1A2, consistent with the altered profile of urinary metabolites. However, both teas caused slight induction of cytochrome P4501A2 versus 1A1, which would be predicted to enhance the activation of IQ. Thus, green tea and black tea are likely to protect against IQ-DNA adducts and ACF by mechanisms other than induction of cytochromes P450, such as inhibition of enzymes which activate IQ or the scavenging of reactive intermediates.

Journal

CarcinogenesisOxford University Press

Published: Jul 1, 1996

There are no references for this article.