Ascorbic acid-induced regression of amyloidosis in experimental animals.
Ascorbic acid was found to accelerate amyloid degradation in an experimental animal model. Based on experiments in vitro which demonstrated the ability of ascorbic acid to restore the amyloid-degrading activity of amyloidotic human serum, the effect of orally administered ascorbic acid was tested in casein-induced murine amyloidosis. Histopathological examination of splenic tissue of mice killed at different times after the termination of the amyloidogenic stimulus showed a markedly decreased amyloid deposition in ascorbic acid-treated animals as compared to the controls. The effect of ascorbic acid was to a certain degree dose-dependent. Colchicine blocked amyloid synthesis when administered during amyloid induction. In animals which were given the drug during the post-induction period it had no effect. The amyloid-degrading activity of mouse serum was reduced in amyloidotic mice. Administration of ascorbic acid partially restored the amyloid-degrading activity of these animals.
D000686:Amyloidosis / Q000188:drug therapy* / Q000473:pathology; D000818:Animals; D001205:Ascorbic Acid / Q000627:therapeutic use*; D003078:Colchicine / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D051379:Mice; D013154:Spleen / Q000473:pathology; D013158:Splenic Diseases / Q000188:drug therapy
D001205:Ascorbic Acid; D003078:Colchicine