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在半乳糖胺处理的大鼠中,去唾液酸糖蛋白特异性肝结合蛋白减少,血清去唾液酸糖蛋白蓄积。

Decrease of a hepatic binding protein specific for asialoglycoproteins with accumulation of serum asialoglycoproteins in galactosamine-treated rats.

作者信息

Sawamura T, Kawasato S, Shiozaki Y, Sameshima Y, Nakada H, Tashiro Y

出版信息

Gastroenterology. 1981 Sep;81(3):527-33.

PMID:7250640
Abstract

Acute liver injury was induced experimentally in rats by a single injection of a large amount of D-galactosamine. Hepatocellular damage was apparent from decrease of total serum proteins, marked release of transaminases into the circulation, precipitous decrease of total microsomal proteins, and intracellular enzymes such as cytochrome P450 and 5'-nucleotidase. In parallel with such hepatocellular damage, serum asialoglycoproteins accumulated markedly, reaching a maximum level 4 days after the injection and then decreased to the control level. In contrast to this increase, hepatic binding protein, a receptor in the liver which specifically recognizes asialoglycoproteins, decreased very much. At the same time, survival time of [125I]asialoorosomucoid intravenously administered into rats was much prolonged in inverse proportion to the decrease of the binding protein. From these results it was concluded that the decrease of the hepatic binding protein induced by galactosamine treatment is probably responsible for the marked accumulation of serum asialoglycoproteins.

摘要

通过单次注射大量D-半乳糖胺在大鼠中实验性诱导急性肝损伤。从血清总蛋白减少、转氨酶大量释放到循环中、微粒体总蛋白急剧减少以及细胞色素P450和5'-核苷酸酶等细胞内酶的变化可以明显看出肝细胞损伤。与这种肝细胞损伤同时发生的是,血清去唾液酸糖蛋白显著积累,在注射后4天达到最高水平,然后降至对照水平。与这种增加相反,肝脏结合蛋白(肝脏中特异性识别去唾液酸糖蛋白的一种受体)大量减少。同时,静脉注射给大鼠的[125I]去唾液酸血清类黏蛋白的存活时间与结合蛋白的减少成反比,大大延长。从这些结果可以得出结论,半乳糖胺处理诱导的肝脏结合蛋白减少可能是血清去唾液酸糖蛋白显著积累的原因。

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