ASPARTATE-AMINOTRANSFERASE, MALATE-DEHYDROGENASE, AND PYRUVATE-CARBOXYLASE ACTIVITIES IN RAT CEREBRAL SYNAPTIC AND NONSYNAPTIC MITOCHONDRIA - EFFECTS OF INVITRO TREATMENT WITH AMMONIA, HYPERAMMONEMIA AND HEPATIC-ENCEPHALOPATHY
ASPARTATE-AMINOTRANSFERASE, MALATE-DEHYDROGENASE, AND PYRUVATE-CARBOXYLASE ACTIVITIES IN RAT CEREBRAL SYNAPTIC AND NONSYNAPTIC MITOCHONDRIA - EFFECTS OF INVITRO TREATMENT WITH AMMONIA, HYPERAMMONEMIA AND HEPATIC-ENCEPHALOPATHY
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DOI：
10.1007/bf00996918
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发表时间：
1991-12-01
影响因子：
3.6
通讯作者：
ALBRECHT, J
中科院分区：
文献类型：
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作者：
FAFFMICHALAK, L;ALBRECHT, J
本研究观察了氯化铵体外治疗、硫代乙酰胺（TAA）肝衰竭引起的肝性脑病（HE）和静脉注射给药引起的慢性高氨血症的影响。在大鼠脑突触和非突触线粒体中检测了醋酸铵给药对两种苹果酸-天冬氨酸穿梭酶：天冬氨酸转氨酶（AAT）、苹果酸脱氢酶（MDH）活性以及对丙酮酸羧化酶（PC）活性的影响。关于穿梭酶的铵离子在体外（3 mM NH 4Cl）的反应中观察到的nonsynaptic线粒体，并表现为AAT活性下降27%，MDH活性下降16%。相比之下，这两种体内条件主要影响突触线粒体酶：TAA诱导的HE产生突触线粒体AAT减少26%和突触线粒体MDH减少50%。高氨血症抑制突触线粒体AAT的30%和突触线粒体MDH的45%。HE在非突触线粒体中没有产生任何影响，而高氨血症使AAT活性增加30%，但MDH没有变化。所有的实验条件影响非突触线粒体PC：氯化铵在体外产生了20%的减少，TAA诱导的HE -30%的减少，其中-作为高氨血症抑制酶的53%。突触线粒体中的PC活性非常低（约为非突触线粒体中测量的2%），这与该酶主要定位于星形胶质细胞一致。
The effects of in vitro treatment with ammonium chloride, hepatic encephalopathy (HE) due to thioacetamide (TAA) induced liver failure and chronic hyperammonemia produced by i. p. administration of ammonium acetate on the activity of the two malate-aspartate shuttle enzymes: aspartate aminotransferase (AAT), malate dehydrogenase (MDH), and on the pyruvate carboxylase (PC) activity were examined in synaptic and nonsynaptic mitochondria from rat brain. With regard to the shuttle enzymes the response to ammonium ions in vitro (3mM NH4Cl) was observed in nonsynaptic mitochondria only, and was manifested by a 27% decrease of AAT activity and a 16% decrease of MDH activity. By contrast, both in vivo conditions primarily affected the synaptic mitochondrial enzymes: TAA-induced HE produced a 26% decrease of synaptic mitochondrial AAT and a 50% decrease of synaptic mitochondrial MDH. Hyperammonemia inhibited synaptic mitochondrial AAT by 30% and synaptic mitochondrial MDH by 45%. HE produced no effect at all in nonsynaptic mitochondria while hyperammonemia produced a 30% increase in the AAT activity, but no changes in MDH. All the experimental conditions affected the nonsynaptic mitochondrial PC: ammonium chloride in vitro produced a 20% decrease, TAA-induced HE - a 30 % decrease, where-as hyperammonemia inhibited the enzyme by 53%. The PC activity in synaptic mitochondria was very low (about 2% of that measured in nonsynaptic mitochondria), which is consistent with the primarily astrocytic localization of the enzyme.