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S-腺苷-L-甲硫氨酸对硫代乙酰胺诱导的大鼠肝损伤的影响。

Effect of S-adenosyl-L-methionine on thioacetamide-induced liver damage in rats.

作者信息

Osada J, Aylagas H, Sanchez-Vegazo I, Gea T, Millan I, Palacios-Alaiz E

出版信息

Toxicol Lett. 1986 Jul-Aug;32(1-2):97-106. doi: 10.1016/0378-4274(86)90054-8.

Abstract

S-Adenosyl-L-methionine (Ado-met) administration to rats significantly improved liver necrosis induced by thioacetamide (TAA) as evidenced by reduction of TAA-elevated catalytic activity of serum aspartate aminotransferase (AST) and alanine aminotransferase (ALAT). Ado-met, however, was not effective in reduction of catalytic activity of serum alkaline phosphatase (ALP) which increased as a consequence of TAA administration. Histologic analysis of the livers supported the biochemical data. Hepatocellular damage was evident from the first day of TAA treatment at daily (i.p.) doses of 50 mg/kg body wt. Maximal necrosis was apparent after 3 days of TAA administration. When rats were treated once a day, for 3 days with Ado-met (2 mg/kg body wt) as well as with TAA, significant reduction of hepatic necrotic area was observed. A similar effect was obtained when doses of 200 mg/kg body wt. of Ado-met were utilized.

摘要

给大鼠施用S-腺苷-L-甲硫氨酸(Ado-met)可显著改善硫代乙酰胺(TAA)诱导的肝坏死,血清天冬氨酸氨基转移酶(AST)和丙氨酸氨基转移酶(ALAT)的催化活性升高是TAA所致,而Ado-met可使其降低,这证明了上述改善作用。然而,Ado-met对降低血清碱性磷酸酶(ALP)的催化活性无效,该酶活性因施用TAA而升高。肝脏的组织学分析支持了生化数据。在以每日腹腔注射50mg/kg体重的剂量给予TAA治疗的第一天,肝细胞损伤就很明显。TAA给药3天后出现最大程度的坏死。当大鼠每天接受一次Ado-met(2mg/kg体重)和TAA治疗,持续3天时,观察到肝坏死面积显著减少。当使用200mg/kg体重的Ado-met剂量时,也获得了类似的效果。

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