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Antimutagenic Potential of Aqueous Tea Extracts towards Selected Environmental Carcinogens: Mechanisms.

Bu-Abbas, Ali H. (1997) Antimutagenic Potential of Aqueous Tea Extracts towards Selected Environmental Carcinogens: Mechanisms. Doctoral thesis, University of Surrey (United Kingdom)..

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Extensive laboratory studies established unequivocally that green tea effectively protects against chemical carcinogenesis. In the present study the ability of tea, both green and black, to modulate the initiation stage of carcinogenesis was investigated. Aqueous extracts of green tea caused a marked inhibition of the mutagenicity of model chemical carcinogens. Two mechanisms were responsible for this effect, namely the inhibition of the cytochrome P450-dependent bioactivation of the carcinogens, and scavenging of the reactive intermediates. A comparison of the antimutagenic potential of green, black and decaffeinated black tea revealed that all three types of tea were effective antimutagens and no difference in potency was evident.In order to evaluate the role of flavanols in the antimutagenic potential of green tea, aqueous extracts were fractionated into four distinct fractions, each of which was fully defined with respect to its content of individual flavanols. The ability of each fraction to antagonise the mutagenicity of model carcinogens could not be correlated with any of the tea flavanols indicating that these compounds are unlikely to play a major role in the antimutagenic effect of green tea. Exposure of rats to green tea aqueous extracts (2. 5 %, w/v) for four weeks stimulated the hepatic O-dealkylation of ethoxy-, methoxy- and pentoxy-resorufin, lauric acid hydroxylation, and increased the apoprotein levels of CYP1A2 and CYP4A1. The same treatment enhanced peroxisomal palmitoyl Co A oxidation and the apoprotein levels of the trifunctional protein in liver homogenate. Of the Phase II enzyme systems studied, treatment with green tea enhanced only the glucuronidation of 2-aminophenol. The O-demethylation of methoxyresorufin and CYP1A2 levels were also induced by black tea, but not by decaffeinated black tea indicating that caffeine is most likely responsible for the increase in the expression of this cytochrome P450 protein. Similarly, the glucuronidation of 2-aminophenol was elevated following treatment with black tea but not black decaffeinated tea.

Item Type: Thesis (Doctoral)
Divisions : Theses
Authors : Bu-Abbas, Ali H.
Date : 1997
Additional Information : Thesis (Ph.D.)--University of Surrey (United Kingdom), 1997.
Depositing User : EPrints Services
Date Deposited : 24 Apr 2020 15:27
Last Modified : 24 Apr 2020 15:27

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