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Genetic Influences on Response to Castration of Liver Growth and Hepatoma Formation¹

The Institute for Cancer Research, 7701 Burholme Avenue, Fox Chase, Philadelphia, Pennsylvania 19111

The effect of castration on liver weight and composition was studied in various mouse genotypes which differ in their susceptibility to formation of spontaneous hepatomas.

In the YS strain, the lethal yellow (A^y) gene induced an increase, in comparison with their intact siblings, in fat-free dry weight of the liver in castrated males. Castration did not affect liver weight of the nonyellow (a/a) YS/ChWf males. Fat-free dry carcass weight of the Ay/a males was not affected by castration, but that of the a/a males was decreased in comparison with their intact siblings. In livers of both genotypes, castration decreased the water content and essentially had no effect on the fat content; however, castration did increase the fat content of the carcasses markedly in both genotypes.

Decreased liver weight as a result of castration was observed in all nonyellow F₁ hybrids carrying the VY strain genome, but in only one yellow (A^vy/A) F₁ hybrid class (BALB/c x VY). The YS strain genome apparently eliminated this response in F₁ hybrid males carrying the hepatoma-resistant BALB/c and C57BL/6 strain genomes. Castration did retard liver weight gain in the inbred BALB/c and C57BL/6 strain males. This effect of castration was not observed in the hepatoma-susceptible C3H strain males.

Ovariectomy of A^y/a and a/a YS females had the same effects on liver and carcass weight as castration of the yellow and nonyellow males of this strain. This and other evidence suggests that the effect of castration on liver weight is not directly induced by decreased levels of sex hormones, but rather by alteration of the hormonal balance.

¹ This work has been supported by USPHS Grants CA-06927 and FR-05539 from the NIH, and by an appropriation from the Commonwealth of Pennsylvania.

Received 12/22/69. Accepted 2/ 5/70.

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