Oxidative/nitrosative stress and hepatic encephalopathy

Abstract Hepatic encephalopathy (HE) is a neuropsychiatric syndrome that frequently occurs in the course of acute or chronic liver diseases. HE is triggered by a heterogeneous group of factors such as ammonia, which is considered a main toxin in HE; hyponatremia; proinflammatory cytokines; and benzodiazepines. Symptoms of HE mainly comprise disturbances of cognitive and motoric function. HE in patients with liver cirrhosis is seen as the clinical manifestation of a low-grade cerebral edema and accompanying cerebral oxidative/nitrosative stress, which trigger a variety of functional consequences. These include posttranslational protein modifications such as tyrosine nitration and O-GlcNAcylation of proteins, oxidation of RNA, gene and protein expression changes, and senescence. It is assumed that these alterations impair the functions of astrocytes and neurons leading to disturbances of glio-neuronal communication in the brain with consequences for neurotransmission and oscillatory networks in the brain.