NDLI: Effects of acute hyperammonemiain Vivo on oxidative metabolism in nonsynaptic rat brain mitochondria

Content Provider	Springer Nature Link
Author	Kosenko, Elena Felipo, Vicente Montoliu, Carmina Grisolía, Santiago Kaminsky, Yury
Copyright Year	1997
Abstract	The effects of hyperammonemia inducedin vivo by injecting rats with ammonium acetate on oxidative phosphorylation, malate-aspartate shuttle, some related enzyme activities and metabolite levels in brain mitochondria were studiedex vivo. Rats were found to be either ammonia-sensitive (showing convulsions) or ammonia-resistant (without convulsions) after intraperitoneal injection of ammonium acetate (7 mmol/kg). Ammonium acetate administration to ammonia-sensitive rats led to inhibition of State 3 rates of brain mitochondria utilizing pyruvate, glutamate, isocitrate, and succinate as substrates and to decreased respiratory control index. In brain mitochondria isolated from ammonia-resistant animals, the ammonia-induced effect on such State 3 rates was not observed. In brain mitochondria from hyperammonemic rats without convulsions, a small increase in the activity of malate dehydrogenase was observed: glutamate dehydrogenase, succinate dehydrogenase, and aspartate aminotransferase were not affected. In brain mitochondria from rats with ammonia-induced convulsions, the activities of malate dehydrogenase and succinate dehydrogenase were reduced significantly. Ammonium acetate injection to rats was associated with a 5-fold increase in the brain mitochondrial ammonium ion content and a decrease (ca. 50%) in brain mitochondrial glutamate and aspartate; brain mitochondrial malate and 2-oxoglutarate levels remained unchanged. The rate of the malate-aspartate shuttle in brain mitochondria of hyperammonemic rats was decreased by 20% as compared to corresponding rate in control rats. We conclude that acute administration of ammonium acetate induces serious disturbances in the electron-transport chain, interferences of the malate-aspartate shuttle, alterations of the levels of shuttle intermediates and inhibition of the activities of malate and succinate dehydrogenases in brain mitochondria.
Starting Page	69
Ending Page	82
Page Count	14
File Format	PDF
ISSN	08857490
Journal	Metabolic Brain Disease
Volume Number	12
Issue Number	1
e-ISSN	15737365
Language	English
Publisher	Springer US
Publisher Date	1997-01-01
Publisher Place	Boston
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Ammonia brain mitochondria malate-aspartate shuttle hyperammonemia Neurosciences Neurology Oncology Biochemistry
Content Type	Text
Resource Type	Article
Subject	Biochemistry Neurology (clinical) Cellular and Molecular Neuroscience

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