Ornithine decarboxylase lability in 2 transplantable highly deviated rat hepatomas.
A strong ornithine decarboxylase (ODC)-inactivating capacity has been previously shown (M.F. Zuretti and E. Gravela (1983) Biochim. Biophys. Acta, 742, 269-277) to be bound to rat liver microsomes. Present results show that in 2 fast-growing transplantable tumors, the 3924A Morris hepatoma and the AH 130 Yoshida ascites hepatoma, microsomes are endowed with a greatly enhanced ODC-inactivating capacity, and, concurrently, ODC displays an extreme in vitro liability and an unusual thiol-dependency (most of the activity requires dithiothreitol supply to be determined). These data are at variance with those previously obtained in hepatomas induced by N-2-fluorenylacetamide (E. Gravela et al., (1983) Cancer Res., 42, 2298-2300). The possibility that ODC liability in the 2 hepatomas here studied may result from in vivo exposure to a strong microsomal activity is considered.
D000818:Animals; D003600:Cytosol / Q000201:enzymology / Q000378:metabolism; D004229:Dithiothreitol / Q000494:pharmacology; D008114:Liver Neoplasms, Experimental / Q000201:enzymology* / Q000378:metabolism; D008297:Male; D008862:Microsomes, Liver / Q000187:drug effects / Q000201:enzymology* / Q000378:metabolism; D009955:Ornithine Decarboxylase / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains
D009955:Ornithine Decarboxylase; D004229:Dithiothreitol