[Tumor-seeking mechanisms of labeled compounds].
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Biomedical subjects
Publications and source records attributed to I N Kendysh.
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A study was made of the intensity of lipid synthesis in the liver and adipose tissue of rats following a single administration of hydrocortisone (3, 6, 24 and 48 hours) from various labeled precursors. In the liver the hormone stimulated the synthesis of lipids from the acetate-I-C14 and lactate 1,3-C14 but blocked the lipogenesis from glycerine-1,2-C14 and glucose-1-c14. In the adipose tissue hydrocortisone intensified the lipid synthesis from glucose-1-C14 only and inhibited the lipid synthesis from other precursors. The action mechanism of the hormone on the lipogenesis is considered in association with the primary intensification of gluconeogenesis in the liver.
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125I-p-iodophenyllaurate proved to be a suitable substrate of lipase for studies of pancreas lipolytic function in vivo and in vitro. After peroral administration into rats the drug was hydrolyzed by lipase. The liberated 125I-p-iodophenol was absorbed in intestine and excreted with urine either as free 125I-p-iodophenol or its conjugates. Activity of pancreatic lipase was measured on the basis of radioactivity estimation of urine per min.
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Dynamics of distribution and excretion with urine of 125I-p-iodophenamine were studied impairment of rat liver tissue microsomal oxidation by means of CC14 treatment. This poison inhibited distinctly metabolism and excretion of the labelled compound in rats but not in rabbits, which was due to difference in the mechanisms of the compound biotransformation. The requirements for compounds suitable for studies of microsomal oxidation by means of excretory test were not met by 125I-p-iodophenamine.
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