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College of Pharmacy, University of Minnesota, Minneapolis, Minnesota 55455 [Y. J. A.], and Department of Biochemistry, Howard University College of Medicine, Washington, D. C. 20001 [H. P. M.]
The activity of estrogen 16
-hydroxylase was measured for nine Morris hepatomas of different growth rates and host livers. Activity was measured in the microsomal fraction of the cell (100,000 x g).
In the spectrum of hepatomas studied, 16
-hydroxylase activity was significantly decreased in parallel with the increase in hepatoma growth rate. The decrease in enzymic activity ranged from 16 to 19% for the slow-growing tumors (Hepatomas 44, 28A, and 9633), 2 to 9% for the intermediate-growing tumors (Hepatomas 38B, 7795, and 5123A), and 0% for the fast-growing tumors (Hepatomas 7288C, 7777, and 42A).
Estrogen 16
-hydroxylase activity of the liver of tumor-bearing rats differed from that of liver of healthy animals. There was a decrease in enzymic activity ranging from 66% to 90% of normal control rats. The activity level of the host liver did not correlate with tumor growth rate.
Stimulation of 16
-hydroxylase with phenobarbital showed a 4-fold increase in activity in normal liver and only a 2- to 3-fold increase in host livers. The slow- and intermediate-growing hepatomas showed a 1.2- to 1.4-fold increase in enzyme activity, and no activity or stimulation in the fast-growing hepatomas was observed.
1 This research was supported in part by the Graduate School, University of Minnesota, Minnesota Medical Foundation, Grant 0694-5813.
2 To whom requests for reprints should be addressed, at the College of Pharmacy, University of Minnesota, Minneapolis, Minn. 55455.
3 Recipient of USPHS Research Grant CA 10729.
Received 7/ 2/76. Accepted 1/10/77.
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