Panova N G, Axenova L N, Medvedev A E
Institute for Biomedical Chemistry, Russian Academy of Medical Sciences, Pogodinskaya str. 10, Moscow, 119832 Russia.
Neurobiology (Bp). 2000;8(3-4):225-30.
The effect of ethanol consumption on the sensitivity of rat brain mitochondrial monoamine oxidases to the inhibition by pargyline in vivo and in vitro was investigated. Administration of pargyline (10 mg/kg, s.c.) produced significantly higher inhibition of MAO-A in alcoholised rats, whereas MAO-B inhibition did not differ from that observed in control animals. The concentration-response curve for the inhibition of brain mitochondrial MAO-A and MAO-B by pargyline in vitro did not reveal higher sensitivity of MAO from alcoholised rats to pargyline. This probably means that more pronounced inhibition by pargyline of brain MAO-A in alcoholised rats in vivo can be attributed to decreased content of compounds reversibly interacting with the its catalytic site. Taking into consideration some ethanol-induced decrease of brain tribulin content we suggest that the reduced level of endogenous inhibitors (tribulin components?) may have some importance in the development of alcoholism.
研究了乙醇摄入对大鼠脑线粒体单胺氧化酶在体内和体外对帕吉林抑制敏感性的影响。皮下注射帕吉林(10mg/kg)对酒精处理的大鼠体内单胺氧化酶A(MAO-A)的抑制作用明显更高,而对单胺氧化酶B(MAO-B)的抑制作用与对照动物无差异。体外实验中,帕吉林对脑线粒体MAO-A和MAO-B抑制作用的浓度-效应曲线未显示酒精处理大鼠的MAO对帕吉林有更高的敏感性。这可能意味着,在体内酒精处理的大鼠中,帕吉林对脑MAO-A的更明显抑制作用可归因于与其催化位点可逆相互作用的化合物含量降低。考虑到乙醇诱导的脑微管蛋白含量有所下降,我们认为内源性抑制剂(微管蛋白成分?)水平降低可能在酒精中毒的发生发展中具有一定作用。