Inhibition of spermidine formation in rat liver and kidney by methylglyoxal bis(guanylhydrazone).
Inhibition of spermidine formation in rat liver and kidney by methylglyoxal bis(guanylhydrazone).
复制标题
甲基乙二醛双（脒腙）抑制大鼠肝脏和肾脏中亚精胺的形成。
作者：
A. Pegg
研究了甲基乙二醛（鸟酰腙）对肝脏和肾脏多胺代谢的影响。甲基乙二醛是一种已知的抑制腐胺依赖s -腺苷-l-蛋氨酸脱羧酶的物质。腹腔注射80mg甲基乙二醛（鸟酰腙）/kg体重至8h后，腐胺向亚精胺的掺入几乎完全被抑制。然而，在给药后20h，亚精胺合成恢复。在此期间，腐胺的积累相当可观（在两个组织中高达对照浓度的3倍），但亚精胺含量仅略有下降。以上结果表明，腐胺激活的s -腺苷-l-蛋氨酸脱羧酶在大鼠肝脏和肾脏的亚精胺生物合成中起着重要作用，并探讨了利用甲基乙二醛（鸟酰腙）研究多胺合成在生长中的作用的可能性。
The effect of methylglyoxal bis(guanylhydrazone), a substance known to inhibit putrescine-dependent S-adenosyl-l-methionine decarboxylase, on polyamine metabolism in liver and kidney was investigated. Almost complete inhibition of the incorporation of putrescine into spermidine was obtained up to 8h after administration of 80mg of methylglyoxal bis(guanylhydrazone)/kg body wt. by intraperitoneal injection. However, by 20h after administration of the inhibitor spermidine synthesis was resumed. Considerable accumulation of putrescine occurred during this period (up to 3 times control concentrations in both tissues), but there was only a slight fall in the spermidine content. These results suggest that the putrescine-activated S-adenosyl-l-methionine decarboxylase plays an essential role in spermidine biosynthesis in rat liver and kidney, and the possibility of using methylglyoxal bis(guanylhydrazone) to study the role of polyamine synthesis in growth is discussed.