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Thyroid Hormone Regulation of Mitochondrial -Glycerophosphate Dehydrogenase in Liver and Hepatoma¹

Department of Medicine and Institute of Cancer Research, Francis Delafield Hospital, College of Physicians and Surgeons of Columbia University, New York, New York 10032

The effect of thyroid hormone in rats upon the induction of mitochondrial -glycerophosphate dehydrogenase (LM-GPDH) has been studied in normal liver, in Novikoff hepatoma, in Morris hepatoma 7800, and in host liver of animals bearing Novikoff or Morris hepatomas. Enzyme activities were determined both before and 48 hr after a single i.p. injection of L-triiodothyronine (T₃), 100 µg/100 g body weight. In livers of rats bearing the rapidly growing Novikoff hepatoma, basal enzyme activity is increased 75% over levels in nontumor-bearing controls. By contrast, hepatic enzyme activity in rats bearing the more slowly growing Morris hepatoma does not differ from control levels. In normal animals, administration of T₃ greatly increases activity of LM-GPDH. In livers of animals bearing either Novikoff or Morris hepatomas, enzyme activity after administration of T₃ is similar to levels obtained in livers of normal animals similarly treated.

The activity of LM-GPDH in Novikoff hepatoma, expressed per mg mitochondrial protein, is considerably higher than in liver, and cannot be induced by T₃. In the Morris hepatoma, basal activity is similar to that of normal liver, and is increased 2-fold by T₃. The present study, therefore, indicates that induction of LM-GPDH by thyroid hormone is not demonstrable in the Novikoff hepatoma, is diminished but present in the Morris hepatoma 7800, and is unimpaired in liver of rats bearing either tumor.

¹ This investigation was supported by USPHS Research Grant CA-02332 from the National Cancer Institute, NIH.

² Supported in part by USPHS Training Grant CA-05011. Present address: University of Connecticut McCook Hospital, Hartford, Conn.

Received 11/10/69. Accepted 2/12/70.