Clinical aspects of urea cycle dysfunction and altered brain energy metabolism on modulation of glutamate receptors and transporters in acute and chronic hyperammonemia
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- 作者：Vijayakumar Natesan ; nvkbiochem@yahoo.co.in" class="auth_mail" title="E-mail the corresponding author ; Renuka Mani ; Ramakrishnan Arumugam
- 关键词：N2 ; nitrogen ; NH3 ; ammonia ; Ca2+ ; calcium ; CPS-1 ; carbomyl phosphate synthetase-1 ; OTC ; ornithine transcarbomylase ; ASS-1 ; argininosuccinate synthetase-1 ; ORNT ; ornithine transporter ; HHH ; hyperornithemia ; hyperammonemia ; homocitrullinemia syndrome ; ASL ; argininosuccinate lyase ; GABA ; γ-amino-butyric acid ; CNS ; central nervous system ; mPT ; mitochondrial permeability transition ; HE ; hepatic encephalopathy ; ONS ; oxidative/nitrosative stress ; PTP ; permeability transition pore ; NMDA ; N-methyl-d-aspa
- 刊名：Biomedicine & Pharmacotherapy
- 出版年：2016
- 出版时间：July 2016
- 年：2016
- 卷：81
- 期：Complete
- 页码：192-202
- 全文大小：2345 K
文摘
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Hepatocellular dysfunction results in impaired clearance of ammonium by the liver.
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Urea has low toxicity even at high concentration, in contrast to its precursors, particularly ammonia.
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Glutamine synthesis is altered under several pathological conditions.
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Synaptically released glutamate is removed by uptake into the surrounding astrocytes and it is cycled via the glutamine-glutamate-cycle.
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The glutamate-nitricoxide-cGMP pathway modulates some forms of learning and memory. Additional feasible mechanism for impaired energy metabolism in hepatic encephalopathy (HE) and hyperammonemia is the mitochondrial permeability transition (mPT).