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Acetaminophen‐induced Liver Injury Induces DNA Damage and Activation of Ataxia Telangiectasia Mutated in Mice

Acetaminophen (APAP) is a common analgesic/antipyretic that is widely used throughout the world. At therapeutic doses it is safe but at higher dosages APAP causes acute liver failure (ALF). Drug‐induced liver toxicity is the most common cause of liver damage, accounting for 50% of the cases of liver failure. With the only efficacious form of treatment being liver transplant, it is imperative to find alternative forms of treatment. Gaining a greater understanding of the molecular pathology contributing to the progression of liver failure, we allow insights on methods to enhance patient care and quality of life. Acute liver injury from APAP is associated with increased levels of inflammation, oxidative stress, and hepatic cell death. High levels of oxidative stress damages multiple systems within the cell, most notability the DNA. In response to DNA damage, DNA damage response (DDR) markers are activated leading to cell cycle arrest, DNA repair and the eventual death of the cell if damage is unable to be repaired. Our hypothesis is that the accumulation of DNA damage results in the activation of the DDR, which then aids in driving further progression of APAP‐induced liver injury.