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Hepatocarcinogenesis in rats produced by prolonged feeding of thioacetamide appears as a progressive phenomenon in which morphological changes are associated with important biochemical modifications. It seems most likely that changes in the permeability of cell membrane induced by the carcinogen are responsible for increased intracellular accumulation of Ca²⁺, and for the ensuring of cell injury produced by Ca²⁺ overloading of the mitochondria. This calcification of the mitochondria may play a role in the neoplastic transformation of the cell, especially as far as it concerns metabolic behavior and the genetic specification of the permeability characteristics of the transformed cell membrane. The increased synthesis of acid glycosaminoglycans suggests their involvement in calcium-mediated control of tumor development and growth.

There is strong experimental evidence indicating that a competitive binding of 67Ga³⁺ to Ca²⁺- and Mg²⁺-binding sites rather than a metabolic process is involved in the accumulation of this radioisotope. These observations suggest that in tumors, as well as in other inflammatory and infectious processes, the most important role in ⁶⁷Ga accumulation is played by a higher availability of those binding sites than in normal tissue.

SummaryThe in vivo distribution of 57Co-hematoporphyrin in adenocarcinoma BW10232-bearing mice has been studied. Tumor-bearing and normal animals exhibit similar patterns of radioactivity accumulation. Twenty-four hours after the administration of the radiocompound the ratios tumor to blood and tumor to muscle indicate a potential value of this radioactive porphyrin for the detection of some types of tumor.

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