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Several compensatory mechanisms can counteract these therapeutic interventions, allowing tumor cells to evade their effects

Abbreviations AIF: apoptosis-inducing factor ALF: acute liver failure ALT: alanine aminotransferase APACHE II: acute physiology and chronic health evaluation II APAP: acetaminophen AST: aspartate transaminase ATP: adenosine triphosphate DAMP: damage-associated molecular pattern DILI: drug-induced liver injury EndoG: endonuclease G FDA: Food and Drug Administration GDCA: glycodeoxycolic acid GDH: glutamate dehydrogenase GSH: glutathione HMGB1: high mobility group B1 HPLC: high-pressure liquid chromatography INR: international normalized ratio IV: intravenous JNK: c-Jun-N-terminal kinase KCH: Kings College Hospital KIM 1: kidney injury molecule 1 MELD: model for end-stage liver disease miRNA: microRNA mtDNA: mitochondrial DNA NAC: N -acetyl cysteine NAPQI: N -acetyl-para-benzo-quinone imine nDNA: nuclear DNA NK: natural killer NKT: natural killer T cells PO: oral SFN: sulforaphane SOFA: sequential organ failure assessment SULT: sulfotransferase UGT: UDP-glucoronosyl transferase Declarations Conflict of interest None Authors contributions Contributed to the manuscript by drafting the document, formatting the figures and tables, obtaining permission for use of previously published figures, and performing final editing of the content (EY), contributed to the manuscript by writing content and formatting the tables in the manuscript (AB), contributed to the manuscript by drafting sections of the document (MC), contributed to the manuscript by providing editing comments (MK), contributed to the manuscript by providing critical revision and administration during the manuscript writing (NP).
