Relative activities of methyl methanesulphonate (MMS) as a genotoxin, clastogen and gene mutagen to the liver and bone marrow of Muta™Mouse mice
✍ Scribed by H. Tinwell; P.A. Lefevre; J. Ashby
- Book ID
- 101265351
- Publisher
- John Wiley and Sons
- Year
- 1998
- Tongue
- English
- Weight
- 160 KB
- Volume
- 32
- Category
- Article
- ISSN
- 0893-6692
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✦ Synopsis
The mutagenicity of the rodent carcinogen methyl kg MMS, failed to enhance the mutagenicity of methanesulphonate (MMS) to the liver and bone MMS to the liver, thereby eliminating the possibility marrow of Muta TM Mouse lacZ 0 transgenic mice that MMS produced promutagenic lesions in the was evaluated. A single intraperitoneal (i.p.) dose liver that were not transformed to mutations because of 100 mg/kg MMS gave a strong positive re-of the absence of MMS-induced cell division. In the sponse in the liver UDS and bone marrow micronu-latter experiments, DMN gave a strong mutagenic cleus assays conducted 2 hr and 30 hr, respec-response and 4AAF a weak mutagenic response. tively, after dosing. A single i.p. administration of Possible reasons for this selective mutagenicity of 100 mg/kg of MMS, or five daily administrations MMS (DNA damage and micronuclei induction in of 20 mg/kg MMS, failed to increase significantly the absence of gene mutations) are discussed, but the lacZ 0 r lacZ / mutation frequency (MF) in either no clear outcome emerges. It is concluded that the liver or the bone marrow, albeit some evidence transgenic mutation assays should not be employed of weak mutagenicity was observed for the liver. for defining genetic toxicity in vivo, but rather The gene mutation analyses were undertaken 14 should be reserved for mechanistic studies on predays after the final chemical exposure. Administra-viously established rodent genotoxins and/or cartion of the liver mitogens dimethylnitrosamine cinogens.