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56 It has also been reported that in fulminant hepatic failure, toxic substances released from the necrotic hepatic remnant and lack of detoxification of substances from the gut inhibit or delay liver regeneration and the recovery of hepatic function including aminotransferase production

82 MTX has been proposed to participate in the process of folate antagonism, adenosine signaling, the blocking of methyl-donor production involved in reactive oxygen species, downregulation of the adhesion-molecule expression, modification of cytokine profiles, and the downregulation of eicosanoids and MMPs

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