Control of δ-Aminolevulinic Acid Synthetase and Tyrosine Aminotransferase in Tumors and Livers of Tumor-Bearing Rats2

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Abstract
Administration of allylisopropylacetamide (AIA) increased the levels of δ-aminolevulinic acid synthetase (ALAS) and tyrosine aminotransferase (TAT) in rat liver. Induction of these enzymes was measured in the tumors and livers of rats bearing Morris hepatomas 5123, 7288C-TC, 7777, 7800, 7794A; Walker carcinosarcoma 256; Fibrosarcoma 4956; and Snell hepatoma 648. a) ALA synthetase was low and not inducible in any tumors studied; b) in livers of tumor-bearing rats, basal levels and peak-induced levels of ALA synthetase were decreased below those seen in normals; c) TAT levels were variable in the tumors, and the enzyme was clearly induced in 4 of the 8; and d) in host livers, basal TAT levels and induced levels were as high as or higher than in controls. Failure to observe induction of ALAS in the tumors did not result from the presence of an inhibitor. Hepatic ALA synthetase induction is known to be blocked by heme and certain carbohydrates (“glucose effect” ). Evidence was obtained indicating that the damped induction of host hepatic ALA synthetase was not caused by heme or lactate released from tumors.

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