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Genetic analysis of liver catalase activity in two substrains of C57BL mice

Published online by Cambridge University Press:  14 April 2009

W. E. Heston ,
Harold A. Hoffman  and
Miloslav Rechcigl Jr
W. E. Heston
Affiliation:
Laboratory of Biology and Laboratory of Biochemistry, National Cancer Institute, National Institutes of Health, Bethesda, Maryland*
Harold A. Hoffman
Affiliation:
Laboratory of Biology and Laboratory of Biochemistry, National Cancer Institute, National Institutes of Health, Bethesda, Maryland*
Miloslav Rechcigl Jr
Affiliation:
Laboratory of Biology and Laboratory of Biochemistry, National Cancer Institute, National Institutes of Health, Bethesda, Maryland*
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The level of liver catalase activity in substrain C57BL/6 mice is only approximately half that in substrain C57BL/He. That this difference was due to a single major gene with low level of activity dominant to high was indicated by analysis of the F1, F2, and backcross hybrids and confirmed by progeny tests of first back-cross male segregants. The gene symbol Ce is suggested.

The absence of any difference between reciprocal hybrids indicated no extra-chromosomal maternal influence.

There was no evidence that this gene controlling liver catalase had any influence on the level of kidney catalase activity for this did not vary between the two parent substrains or the hybrid groups.

Males consistently had higher liver and kidney catalase activity than females. The difference was more pronounced in respect to kidney catalase, males having about twice the activity found in females.

Type
Research Article
Information
Genetics Research , Volume 6 , Issue 3 , November 1965 , pp. 387 - 397
Copyright
Copyright © Cambridge University Press 1965

References

REFERENCES

Beers, R. F. Jr, & Sizer, I. W. (1952). A spectrophotometric method for measuring the breakdown of hydrogen peroxide by catalase. J. biol. Chem. 195, 133–140.CrossRefGoogle ScholarPubMed
Boyer, P. D. & Segal, H. L. (1954). Sulfhydryl groups of glyceraldehyde-3-phosphate dehydrogenase and acyl-enzyme formation. In The Mechanism of Enzyme Action (McElroy, W. D. & Glass, B., eds.), pp. 520–532. Baltimore: The Johns Hopkins Press.Google Scholar
Geisser, S. (1964). Posterior odds for multivariate normal classifications. J. R. statist. Soc, Series B, 26, 69–76.Google Scholar
Greenstein, J. P. & Andervont, H. B. (1942). The liver catalase activity of tumor bearing mice and the effect of spontaneous regression and of removal of certain tumors. J. natn. Cancer Inst. 2, 345–355.Google Scholar
Hamilton, H. B. & Neel, J. V. (1963). Genetic heterogeneity in human acatalasia. Am. J. hum. Genet. 15, 408–419.Google ScholarPubMed
Heston, W. E. (1949). Development of inbred strains in the mouse and their use in cancer research. In Roscoe B. Jackson Memorial Laboratory's 20th Commemoration Lectures on Genetics, Cancer, Growth, and Social Behavior. Bar Harbor, Maine; Bar Harbor Times.Google Scholar
Heston, W. E., Vlahakis, G. & Deringer, M. K. (1960). High incidence of spontaneous hepatomas and the increase of this incidence with urethan in C3H, C3Hf, and C3He male mice. J. natn. Cancer Inst. 24, 425–435.Google ScholarPubMed
Rechcigl, M. Jr, & Heston, W. E. (1963). Tissue catalase activity in several C57BL substrains and in other strains of inbred mice. J. natn. Cancer Inst. 30, 855–864.Google ScholarPubMed
Rechcigl, M. Jr, Price, V. E. & Morris, H. P. (1962). Studies on the cachexia of tumor-bearing animals II. Catalase activity in the tissues of hepatoma-bearing animals. Cancer Res. 22, 874–880.Google ScholarPubMed
Takahara, S., Hamilton, H. B., Neel, J. N., Kobara, T. Y., Ogura, Y. & Nishimura, E. T. (1960). Hypocatalasima, a new genetic carrier state. J. clin. Invest. 39, 610–619.CrossRefGoogle ScholarPubMed