The effect of a liver protein synthesis inhibitor on plasma SAA levels in a model of accelerated amyloid deposition.
Animals treated with AgNO3 and amyloid-enhancing factor deposit large quantities of splenic amyloid in 48 hours. The kinetics of SAA production was examined in such a model in the presence and absence of an inhibitor of liver protein synthesis (ethionine). Ethionine had little effect on splenic protein synthesis but inhibited both the production of SAA and liver protein synthesis. When experiments were performed with fed mice, ethionine induced an inhibition of liver protein synthesis lasting 16 hours. Thereafter, liver protein synthesis began to recover, accompanied by a rise in plasma SAA levels. These results are consistent with hepatic but not splenic synthesis of SAA.
D000682:Amyloid / Q000097:blood* / Q000378:metabolism*; D000818:Animals; D004435:Eating; D005001:Ethionine / Q000494:pharmacology*; D005260:Female; D008099:Liver / Q000378:metabolism*; D051379:Mice; D008808:Mice, Inbred CBA; D008954:Models, Biological; D014176:Protein Biosynthesis; D000685:Serum Amyloid A Protein / Q000096:biosynthesis / Q000097:blood*; D012835:Silver Nitrate / Q000494:pharmacology; D013154:Spleen / Q000378:metabolism
D000682:Amyloid; D000685:Serum Amyloid A Protein; D012835:Silver Nitrate; D005001:Ethionine