The pathogenesis of hepatic encephalopathy (HE) remains elusive. While it is clear that ammonia is the likely toxin and that astrocytes are the main target of its neurotoxicity, precisely how ammonia brings about cellular injury is poorly understood. Studies over the past decade have invoked the concept of oxidative stress as a pathogenetic mechanism for ammonia neurotoxicity. This review sets out the arguments in support of this concept based on evidence derived from human observations, animal studies, and cell culture investigations. The consequences and potential therapeutic implications of oxidative stress in HE are also discussed.
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