An Experimental Study on the Chemopreventive effect of Chlorophyllin in Hamster Cheek Pouch Tumor induced by 7, 12-dimethylbenzaanthracene.
- Author:
Kyu Ho YOON
1
Author Information
1. Department of Oral & Maxillofacial Surgery, College of Medicine, Inje University.
- Publication Type:Original Article
- Keywords:
Chemoprevention;
DMBA;
Mutation;
Non-isotopic restriction fragment length polymorphism Tumor yield
- MeSH:
9,10-Dimethyl-1,2-benzanthracene;
Animals;
Carcinogenesis;
Carcinogenicity Tests;
Cheek*;
Chemoprevention;
Chlorophyll;
Codon;
Copper;
Cricetinae*;
Drug Therapy;
Genes, ras;
Histidine;
Mutagenicity Tests;
Mutation Rate;
Polymerase Chain Reaction;
Polymorphism, Restriction Fragment Length;
Sodium
- From:Journal of the Korean Association of Oral and Maxillofacial Surgeons
2000;26(2):137-145
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Carcinogenesis is a multi-stage process that generally consists of at least three steps; initiation, promotion, and progression. If one of these carcinogenic steps were suppressed or delayed, the cancer could be prevented. Cancer chemoprevention is defined to be inhibition or reversal of the carcinogenic process by the specific chemical agents and is a novel approach to cancer management alternative to conventional chemotherapy. Chlorophylln(CHL), a water-soluble derivative of chlorophyll, containing sodium and copper, has been known to be strong antimutagen in several test systems, but its mechanism of antimutagenic action is unknown. In the present experiment, the possibility of CHL as chemopreventive drugs on 7,12-dimethylbenz[a]anthracene(DMBA)-induced hamster buccal pouch carcinogenesis was investigated by mutagenicity test, carcinogenicity test, and frequency or spectrum of H-ras mutations in the both of DMBA-induced and chlorophylln-pretreated-DMBA induced tumor by polymerase chain reaction and non-isotopic restriction fragment length polymorphism. The treatment of CHL reduced the yields and multiplicity of the 0.5% DMBA-induced tumor, 86% to 62.5% and 3.7+/-0.6 to 1.4+/-0.3, respectively. The occurrence of histidine revertant by 20 micromole DMBA was inhibited 25.6 to 81.7% by 1 to 5 microM CHL in a dose-dependent manner. The mutation rates of H-ras gene in DMBA-induced and CHL-pretreated-DMBA induced tumor were 96%, 94% of which the most mutations were in codon 12/13. These results suggest that CHL inhibits the carcinogenic action of DMBA by the formation of complex between CHL and DMBA or the inhibition of the activation of DMBA in vivo. But CHL did not affect the mutation rates or its spectrum in already formed tumor.
