A Review of Bioinformatics Tools to Understand Acetaminophen-Alcohol Interaction.

摘要: Background: Drug-ethanol interaction can result in hepatotoxicity. The liver is capable of metabolizing both acetaminophen and ethanol; however, severe acute or moderate chronic simultaneous exposure cause cell tissue damage. Therapeutic doses become harmful if gene activity altered via competition for metabolic pathways. Simultaneous intake ethanol results overactive CYP2E1 depletion glutathione, leaving NAPQI to build up the liver. a hepatotoxic substance typically neutralized by glutathione. Methods: Bioinformatics tools including PharmGKB, Chemical Annotation Retrieval Toolkit, Transcriptome Analysis Console 4.0 (TAC), wikipathways, STRING, Ingenuity Pathway (IPA) were used explore interactive pathways ethanol-acetaminophen as proof concept assessing drug-drug drug-alcohol interactions. Results: As comparison indicates, bioinformatics may be understand following acetaminophen, with potential extrapolation other drug-drug/drug-ethanol Conclusions: Direct effects not able confirmed through this study due lack existing data. This work suggests that battery software applications should assess effects.