Mechanism of inhibition of hepatic protein synthesis in rats by the carcinogen, methylazoxymethanol acetate.

Treatment of rats with the carcinogen, methylazoxymethanol acetate, results in a rapid, marked inhibition of hepatic protein synthesis and disaggregation of polysomes. Studies were undertaken to learn the mechanism by which this carcinogen induces these effects in rat liver. The data show that the inhibition of endogenous protein synthesis is not due to an effect on the high speed supernatant 'factors' but rather at the level of the polysome, and that both free and membrane-bound polysomes are affected. Poly(U)-directed polyphenylalanine synthesis by native ribosomal subunits is greater in preparations isolated from rats treated with carcinogen than it is in controls. Moreover, the native ribosomal subunit fraction from treated livers in response to added rabbit globin mRNA is able to synthesize a protein similar in molecular weight to globin. These studies show that methylazoxymethanol acetate does not induce significant alterations of ribosomal subunits or of initiation factors and suggest that the inhibition of protein synthesis and disaggregation of polysomes may be the results of an alteration of cytoplasmic mRNA, or its association with ribosomes.     

Lactose metabolism by Streptococcus mutans: evidence for induction of the tagatose 6-phosphate pathway.

Growth on lactose by strains of Streptococcus mutans resulted in the induction of the lactose-phosphoenolpyruvate-phosphotransferase system, phospho-beta-galactosidase, and the enzymes of the tagatose 6-phosphate pathway.     

Ochratoxin A-induced iron deficiency anemia.

Ochratoxin A at 8 micrograms per g of diet, but not at lower doses, fed to chickens from 1 day to 3 weeks of age resulted in significantly (P less than 0.05) decreased packed blood cell volume and hemoglobin concentration without altering the number of circulating erythrocytes. Serum iron and percentage of transferrin saturation were lowered at 4 and 8 micrograms/g. Therefore, anemia was characteristic of severe ochratoxicosis of young chickens, and the anemia was categorized as a hypochromic-microcytic anemia of the iron deficiency type. These data indicate that ochratoxin A by itself does not cause hemorrhagic anemia syndrome of chickens and that an anemia caused by a nutritional deficiency can be elicited by a mycotoxin.     

Survey of aflatoxicosis in farm animals.

Over a 22-month period, 278 submissions of farm animals were made to the North Carolina Diagnostic Laboratory for suspected aflatoxicosis, and 94 cases were confirmed on the basis of finding aflatoxin in the feed and the occurrence of bile ductule proliferation. There was an annual variation in the incidence of aflatoxicosis, as well as a seasonal variation: the peak incidence occurred in the winter, and the minimum incidence occurred during the summer. The annual increase coincided with the corn harvest. All confirmed cases occurred on farms that raised and stored their own corn, and 88% were in swine. The cases were geographically localized in the eastern section of North Carolina (94% of the total cases) where 82% of the swine and 79% of the corn are produced. Mean concentration of aflatoxin in feed samples from the confirmed cases was 3,890 mug/kg, and the mean value for corn used in making the feed was 5,180 mug/kg. Only aflatoxin B1 was found in the samples. These data were interpreted to mean that the incidence and severity of aflatoxicosis is greater than previously suspected, that poor on-farm storage of corn is a primary contributing factor, that aflatoxin formation continues during and after the milling process, and that mycotoxicoses other than aflatoxicosis may cause equal or greater problems.     

Comparative effects of estradiol-17beta and estriol on uterine RNA polymerases I, II, and III in vivo.

The early and later effects of estradiol-17β and estriol on the RNA polymerase activities of uterine nuclei obtained from ovariectomized rats were compared. At 4 hr of hormone action both estradiol-17β and estriol stimulated the activity of polymerase I, but not the activities of polymerases II and III. At 24 hr, however, the effect of estriol had disappeared, whereas estradiol-17β stimulated all three polymerase activities. These results indicate that estrogen-induced growth of the uterus occurs in two phases, initiation and maintenance. Estriol initiates uterine growth, but does not maintain the process. Estradiol-17β, in contrast, does both. The differences in the effects of the two estrogens may reside in their different binding affinities.