Braun R, Gerdes T, Steffen C, Netter K J
Arzneimittelforschung. 1982;32(1):59-63.
Gyromitrin, the main poison of the false morel Gyromitra esculenta, causes enlargement of the liver in rats. The content of triglycerides and total cholesterol were increased in the liver homogenate and microsomal fraction but not in the mitochondrial fraction. On the other hand the content of phospholipids was found to be decreased. The enhanced incorporation of [14c]-acetate into the lipids of rat livers after gyromitrin indicates an increased rate of lipids synthesis. The diminution of the phospholipids is caused mainly by a loss of phosphatidyl ethanolamine (PE) although after a short pulse with [14C]-ethanolamine the specific radioactivity of the isolated phosphatidyl ethanolamine corresponded to that of the controls. Since the content of phosphatidylcholine (PC) remained unchanged, the PC/PE-ratio was shifted from 2.3 to 4.5. These effects were reversible within 48 h. Inhibition of the synthesis of highly unsaturated fatty acids by the microsomal monoxygenase system is discussed as the primary reason for the above observations this inhibition possibly being due to active metabolites of gyromitrin which destroy the monoxygenases.
鹿花菌素是鹿花菌(Gyromitra esculenta)的主要毒素,可导致大鼠肝脏肿大。肝脏匀浆和微粒体部分中甘油三酯和总胆固醇的含量增加,但线粒体部分未增加。另一方面,发现磷脂含量降低。鹿花菌素处理后,[14C] - 乙酸盐掺入大鼠肝脏脂质中的量增加,表明脂质合成速率加快。磷脂减少主要是由于磷脂酰乙醇胺(PE)的损失,尽管在用[14C] - 乙醇胺进行短脉冲处理后,分离出的磷脂酰乙醇胺的比放射性与对照组相当。由于磷脂酰胆碱(PC)的含量保持不变,PC/PE比值从2.3变为4.5。这些影响在48小时内是可逆的。微粒体单加氧酶系统对高度不饱和脂肪酸合成的抑制被认为是上述观察结果的主要原因,这种抑制可能是由于鹿花菌素的活性代谢产物破坏了单加氧酶。