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Ribosomes of mouse liver following administration of dimethylnitrosamine.

Summary Administration of dimethylnitrosamine (DMNA), 50 mg/kg, to mice for 2 hr resulted in a 60% inhibition of hepatic protein synthesis. This effect was accompanied by a disaggregation of both free and membrane-bound polysomes. The increased monomers in the membrane-bound fraction remained associated with the membranes. Isolated total monomers from DMNA-treated mice were equivalent to control monomers in their utilization of the synthetic template polyuridylic acid. Also, isolated polysomes from both groups had the same endogenous amino acid-incorporating activity. The lack of a direct action of DMNA on the state of aggregation of polysomes was demonstrated by the finding that cycloheximide, which arrests the readout of polysomes, largely protected the polysomes from disaggregation by DMNA.