L-arginine is required for expression of the activated macrophage effector mechanism causing selective metabolic inhibition in target cells.

作者: R R Taintor , J B Hibbs , Z Vavrin

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摘要: L-Arginine is required for expression of the activated macrophage cytotoxic effector mechanism that causes inhibition mitochondrial respiration, aconitase activity, and DNA synthesis in tumor target cells. This active presence L-arginine even when cocultivation medium lacks all other amino acids serum. Cytotoxic macrophage-induced respiration cells proportional to concentration medium. must be present during period. Pretreatment macrophages with or posttreatment after not effective. D-Arginine does substitute at high concentrations a competitive inhibitor L-arginine-dependent mechanism. Other analogues could replace include agmatine, argininic acid, arginine hydroxamate, tosyl-L-arginine methyl ester. L-homoarginine, however, can effectively L-arginine. NG-monomethyl-L-arginine potent this High lipopolysaccharide do reverse by NG-monomethyl-L-arginine. However, overridden increasing culture We compared NGNG-dimethyl-L-arginine NGN1G-dimethyl-L-arginine as inhibitors The results show inhibitory effect these guanidino methylated derivatives highly determined structure. Guanidine weak requirement appear protein synthesis, creatine biosynthesis, polyamine ADP ribosylation reactions. Bacterial effective second signal only contains L-arginine, strict dependency lipopolysaccharide. Bovine liver arginase, competing medium, inhibits

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