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Hyperammonaemia induces mitochondrial dysfunction and neuronal cell death.

Plamena R Angelova1, Annarein J C Kerbert2, Abeba Habtesion2

  • 1Queen Square Institute of Neurology, University College London, London, UK.

JHEP Reports : Innovation in Hepatology
|July 18, 2022
PubMed
Summary
This summary is machine-generated.

Hyperammonaemia in cirrhosis causes significant brain mitochondrial dysfunction and neuronal injury. An ammonia scavenger partially reversed these effects, suggesting a new mechanism for hepatic encephalopathy.

Keywords:
AmmoniaBDL, bile duct ligationCA1, cornu ammonis 1CA3, cornu ammonis 3CNS, central nervous systemCell deathDG, dentate gyrusDIV, days in vitroETC, electron transport chainFCCP, carbonyl cyanide 4-(trifluoromethoxy) phenylhydrazoneGFAP, glial fibrillary acidic proteinHE, hepatic encephalopathyHEt, dihydroethidiumHepatic encephalopathyLP, lipid peroxidationLiver cirrhosisMitochondrial functionNaCN, sodium cyanideOP, ornithine phenylacetatePI, propidium iodideROI, region of interestROS, reactive oxygen speciesTCA, tricarboxylic acidTMRM, tetramethyl rhodamine, methyl estermPT, mitochondrial permeability transitionΔψm, mitochondrial membrane potential

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Area of Science:

  • Neuroscience
  • Hepatology
  • Biochemistry

Background:

  • Cirrhosis-induced hyperammonaemia is linked to hepatic encephalopathy (HE), with astrocytic swelling as a primary suspect.
  • The specific role of neuronal dysfunction in HE pathogenesis remains unclear.
  • This study investigates the impact of hyperammonaemia on neuronal and astrocyte mitochondrial function.

Purpose of the Study:

  • To explore the effects of hyperammonaemia on mitochondrial function in co-cultures of neurons and astrocytes.
  • To investigate mitochondrial dysfunction in acute brain slices of cirrhotic rats.
  • To assess the therapeutic potential of an ammonia scavenger in mitigating hyperammonaemia-induced brain injury.

Main Methods:

  • Primary co-cultures of neurons and astrocytes were exposed to varying concentrations of ammonium chloride (NH4Cl).
  • Acute brain slices from bile duct ligation (BDL)-induced cirrhotic rats, with and without ornithine phenylacetate (OP) treatment, were analyzed.
  • Live cell imaging techniques measured mitochondrial membrane potential (Δψm), reactive oxygen species (ROS), lipid peroxidation (LP), and cell viability.

Main Results:

  • NH4Cl exposure in neuronal cultures induced mitochondrial dysfunction, increased ROS, and reduced cell viability.
  • BDL-induced cirrhosis in rats elevated cerebral LP and cytosolic ROS, which were normalized by OP treatment.
  • Mitochondrial dysfunction in BDL rats included hyperpolarized Δψm, increased ATP consumption, and elevated mitochondrial ROS; OP treatment restored Δψm.
  • Neuronal loss in the hippocampus of BDL rats was partially prevented by OP administration.

Conclusions:

  • Low-grade hyperammonaemia significantly impairs brain mitochondrial function in cirrhosis.
  • Hyperammonaemia causes profound neuronal injury, partially reversible with ammonia scavenging therapy.
  • These findings reveal a novel mechanism contributing to hepatic encephalopathy development and suggest potential therapeutic targets.