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RESEARCH PRODUCT
In vivo antigenotoxic effects of dietary allyl sulfides in the rat
Corinne RoyM. SuschetetChristine DupontAnne-marie Le Bonsubject
MaleSalmonella typhimuriumCancer ResearchAflatoxin B1[SDV]Life Sciences [q-bio]Allyl compoundMutagenSulfidesmedicine.disease_cause030226 pharmacology & pharmacyDimethylnitrosamineAmes test03 medical and health scienceschemistry.chemical_compound0302 clinical medicineN-NitrosodimethylaminemedicineAnimalsAnticarcinogenic AgentsDisulfidesComputingMilieux_MISCELLANEOUSMutagenicity TestsDiallyl disulfidefood and beveragesAntimutagenic AgentsMethylnitrosoureaRats3. Good healthAllyl Compounds[SDV] Life Sciences [q-bio]LiverOncologychemistryBiochemistry030220 oncology & carcinogenesisRATAllyl MercaptanCARCINOGENESEAllyl SulfideGenotoxicityDNA DamageMutagensdescription
The effects of dietary administration of diallyl sulfide (DAS), diallyl disulfide (DADS) and allyl mercaptan (AM) on the genotoxicity of different chemicals were studied in two experimental systems: (i) measurement of hepatic DNA single-strand breaks induced in rats by aflatoxin B1 (AFB1), N-nitrosodimethylamine (NDMA) or methylnitrosourea (MNU); (ii) mutagenicity of AFB1 or NDMA on Salmonella typhimurium TA100 using hepatic S9 from rats fed allyl sulfides as the activation system. All compounds strongly reduced hepatic DNA breaks induced by AFB1 and NDMA but did not modify the genotoxicity of MNU. In the Ames test, the mutagenicity of NDMA was strongly inhibited by hepatic S9 from rats fed either compound. The mutagenicity of AFB1 was also reduced but to a lesser extent. Such effects are likely related to the modulation of drug-metabolizing enzymes which play a key role in metabolic activation as well as detoxication of NDMA and AFB1.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 1997-01-01 | Cancer Letters |