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Increased concentrations of serum AFP in CCl<SUB>4</SUB>and ethionine-injured rats were primarily due to the increased AFP synthesis<I>de novo</I>in injured liver, secretion of AFP into the blood circulation and AFP catabolism in blood being not altered upon liver injury.<BR>Treatment with a lower dose of thioacetamide resulted in no significant elevation of serum AFP with a markedly increased incorporation of<SUP>3</SUP>H-thymidine into liver DNA without any evidence of liver injury. On the other hand, the administration of ethionine, which caused little necrosis of liver cells, produced increases in serum AFP concentration with no stimulation of hepatic DNA synthesis. The studies on differential effects of mitomycin C and 8-azaguanine on serum AFP levels suggested the presence of different underlying mechanisms of enhanced AFP production for the rats treated with CCl<SUB>4</SUB>and for those after partial hepatectomy. The elevation of serum AFP in liver-injured rats was thus not directly related to the stimulation of hepatic DNA. Some additional mechanisms of specific gene amplification for AFP, which is geared with hepatic injury<I>per se</I>, appear to play a major role in the increased AFP production in injured liver.<BR>Regulatory mechanisms and factors for increased AFP synthesis by hepatic injury was preliminarily investigated. Prednisolone administration inhibited effectively the increased levels of serum AFP in CCl<SUB>4</SUB>and ethionine-treated rats but ATP plus methionine did not, which significantly accelerated the physiological decrease of serum AFP concentrations after birth.
- 財団法人 日本消化器病学会の論文
財団法人 日本消化器病学会 | 論文
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