The effect of dietary protein deficiency on the ability of isolated hepatic microsomes to alter the mutagenicity of a primary and a secondary carcinogen

Czygan, P.; Greim, H.; Garro, A.; Schaffner, F.; Popper, H.

Cancer Research 34(1): 119-123

1974


ISSN/ISBN: 0008-5472
PMID: 4588542
Accession: 000225043

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Abstract
Mice were given a normal or a semisynthetic diet which contained protein 30, 10, 10 and choline-deficient or 3% protein, for 28 days, or a diet free from protein for 7 days; protein and cytochrome P-450 were estimated in liver microsomes. Liver weight and cytochrome P-450 in microsomes fell with decreasing protein in the diet; cytochrome P-450 was further reduced in choline deficiency. Protein in microsomes was increased on the diet with 10% protein which was deficient in choline and was reduced on the diets with 3% or no protein.The secondary carcinogen dimethylnitrosamine at concentrations up to 200 mmol/litre was not mutagenic for Salmonella typhimurium but increased reversion from his- to his+ phenotype resulted when microsomes and NADPH-generating system also were present. The mutagenic effect of DMN in the mixture was greatest with microsomes from mice on diets high in protein, and lowest with microsomes from those on low-protein diets. With the primary carcinogen N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), the results were a complete reversal of those for dimethylnitrosamine (DMN); MNNG was strongly mutagenic, its capacity was present at a concentration of 20 mM, was reduced when all components of the system were present, and was also reduced when microsomes from mice on high-protein diets were present. The activation of DMN and inactivation of MNNG by microsomes were proportional to their cytochrome P-450 content.