MODIFICATION OF HEXOBARBITAL METABOLISM BY MORRIS HEPATOMA 5123tc

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Abstract
Slices of the Morris 5123tc "minimum-deviation" hepatoma fail to metabolize hexobarbital in vitro; slices of non-tumorous liver from the host rats metabolize it at a lower rate than liver slices from normal animals. A corresponding in vivo difference is indicated by a prolonged hexobarbital sleeping time in tumor-bearing rats. The prolongation begins only when the hepatoma becomes large enough to show areas of necrosis or ulceration, and increases steadily with further tumor growth. Surgical removal of the tumor restores the sleeping time to normal. Since the tumor is implanted subcutaneously and does not invade the liver, it is suggested that a diffusible product of tumor necrosis is responsible for the impairment of hexobarbital metabolism in the host liver.