The fate and acute toxicity of aflatoxin B1 in the mastomys and rat.
The fate and acute toxicity of aflatoxin B1 (AFB1) were studied in the mastomys (Praomys coucha) and compared with Fischer rats. The experiment regarding the fate of [3H]AFB1 showed that the radioactivity was excreted mainly through the feces, more rapidly in the mastomys than in the rat, regardless of whether [3H]AFB1 was given orally or intravenously. The levels of radioactivity bound to the liver DNA were lower in the mastomys than in the rat, indicating that the levels of AFB1 binding to the macromolecules in the liver were lower in the mastomys. Consistent with such differences in the fate of AFB1 between the two species, the mastomys were far more resistent to the acute effects of AFB1 than were the rats. Oral administration of AFB1 at a dose of 1.0 mg/kg to rats caused marked microscopic changes in the liver, involving hepatic necrosis and proliferation of bile ducts, but at a dose of 4.0 mg/kg to mastomys caused no pathological changes in the liver or kidneys, and at a dose of 10.0 mg/kg caused only glycogen deposition in hepatic cells in a limited area. The observed differences in susceptibility to the toxic effects of AFB1 and in the fate of AFB1 between the two species are in accord with our previous finding that liver cytosol in the mastomys inhibits microsome-mediated AFB1-DNA binding in vitro more strongly than in rat liver.
Kumagai
S
S
Department of Biomedical Food Research, National Institute of Infectious Diseases, Tokyo, Japan.
Sugita-Konishi
Y
Y
Hara-Kudo
Y
Y
Ito
Y
Y
Noguchi
Y
Y
Yamamoto
Y
Y
Ogura
A
A
D016604:Aflatoxin B1 / Q000493:pharmacokinetics / Q000633:toxicity*; D000818:Animals; D003600:Cytosol / Q000187:drug effects* / Q000378:metabolism; D004351:Drug Resistance; D005243:Feces / Q000737:chemistry; D005978:Glutathione / Q000378:metabolism*; D008297:Male; D009115:Muridae; D051381:Rats; D011916:Rats, Inbred F344; D013045:Species Specificity; D014018:Tissue Distribution
D016604:Aflatoxin B1; D005978:Glutathione