Abstract: Ammonia toxicity has been generally accepted as one of the classic theories of the pathogenesis of hepatic encephalopathy (HE). Ammonia induces changes in neurological system energy metabolism, oxidative stress, mitochondrial permeability transition (MPT), GABA and Glutamatergic neurotransmission, intracellular signal transduction and Aquaporin 4 (AQP4) expression, astrocyte swelling is another important consequence of ammonia neurotoxicity. This article reviewed the role of these factors in the mechanism of HE and ammonia toxicity.

Key words: encephalopathy (HE), ammonia toxicity, oxidative stress, energy metabolism, mitochondrion, review