Induction of oral mucosal tumors in hamsters and rats treated with methyl(acetoxymethyl)nitrosamine.

An oral tumor model has been developed in inbred Syrian golden hamsters by continuous applications every 2 weeks of methyl(acetoxymethyl)nitrosamine [(DMN-OAC) CAS: 56856-83-8; methylnitrosaminomethyl ester acetic acid] at 2 mg/kg body weight alone or by a single application of DMN-OAC followed by continuous twice weekly applications of 12-O-tetradecanoylphorbol 13-acetate (TPA) (1 microgram/animal). Similar studies were done in the W rat buccal mucosa. In the hamsters treated continuously with DMN-OAC, 100% of the tumors were observed in the cheek pouch; none were observed at other sites. In contrast, in the rats treated similarly, only a 67% tumor incidence was observed, of which only 42% were oral tumors. A promoter effect of TPA was observed in hamster cheek pouch tumors induced by DMN-OAC, whereas rat oral mucosa did not respond to TPA treatment.

Mutagenicity and carcinogenicity of mono- and diacetyl hydrazine.

Two hydrazine derivatives, monoacetyl hydrazine (MAH) and diacetyl hydrazine (DAH), have been tested for mutagenic response in the Salmonella/mammalian microsome assay and micronucleus test. MAH but not DAH, increased the revertant mutants in TA100 and TA1535 and also increased the frequency of micronuclei in polychromatic erythrocytes. Gavage administration of MAH but not of DAH, resulted in increased incidence of lung tumors. These observations record for the first time the mutagenicity/carcinogenicity of MAH which is one of the metabolites of isoniazid in animals and humans.

Experimental studies on mutagenic and carcinogenic effects of tobacco chewing.

The alcoholic extract of the chewing (Pandharpuri) variety of tobacco (Nicotiana tabacum) was subjected to mutagenicity and tumorigenicity studies. The extract was found to be mutagenic in strain TA 98 of Salmonella typhimurium in the presence of S 9 mixture. It also induced 8 AZG-resistant mutation in V 79 Chinese hamster cells. Administration of tobacco extract to male Swiss mice by gavage or mixed with diet resulted in an increased incidence of lung/liver tumors. Further, an additive effect of tobacco extract and hexachlorocyclohexane on liver tumor induction was observed.

Chilli extract treatment and induction of eye lesions in hamsters.

On chronic administration of 20 microliter of chilli extract to the cheek pouch of hamsters till death, 23% of the hamsters developed shrunken eye balls and closing of the eyelids. This effect was not observed in hamsters which received a single application of the potent carcinogen methylacetoxymethyl nitrosamine (DMN-OAC) (2 mg/kg body wt.) prior to repeated treatment with chilli extract. Vitamin A levels decreased significantly in the liver tissue of chilli-treated and carcinogen + chilli-treated groups compared to absolute alcohol-treated and untreated groups, while serum Vitamin A values decreased only in the DMN-OAC + chilli-treated group. However, Vitamin A levels do not seem to be linked causally with the effect on the eyes of chilli-treated hamsters, because these hamsters had circulating levels of Vitamin A comparable to those observed in untreated and alcohol-treated groups.

Mutagenicity and carcinogenicity of tea, Camellia sinensis.

Aqueous, caffeine free and tannin fractions of commercial tea and tannic acid were tested for mutagenicity in Ames test. Tea fractions of tannic acid were non mutagenic in strains TA 100, TA 98, TA 1535 and TA 1538 of Salmonella typhimurium with or without metabolic activation (rat-S9 mix) at different doses tested. In strain TA 98 the above tea fractions and tannic acid inhibited the S9 mix mediated mutagenicity of tobacco in a dose dependent manner. The different tea fractions at 60 degrees C, did not increase the tumor incidence in Swiss mice by gavage feeding. They also failed to produce tumors when injected subcutaneously. Caffeine free tea extract decreased the tobacco induced liver tumors but had no effect on lung tumors. The same fraction was ineffective in hexachlorocyclohexane induced liver tumors in Swiss mice.