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Drug-induced liver injury (DILI) is a crucial factor that poses a significant threat to human health. DILI process leads to the changes of reactive oxygen species and reactive nitrogen species content in cells, which leads to oxidative and nitrosative stress in cells. However, the high reactivity of hypochlorous acid (HOCl) and peroxynitrite (ONOO⁻), combined with a lack of in situ imaging techniques, has hindered a detailed understanding of their roles in DILI.

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Genetic and Genomic Approaches to the Study of Drug-Induced Liver Injury.

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Faculty of Medical Sciences, Translational & Clinical Research Institute, Newcastle University, Newcastle upon Tyne, UK.

Idiosyncratic hepatotoxicity induced by prescribed drugs has been known since the early 20th century. Identifying risk factors, including genetic factors, that trigger this drug-induced liver injury (DILI) has been an important priority for many years, both to prevent drugs that cause liver injury being licensed and as a potential means of preventing at-risk patients being prescribed causative drugs. Improved methods for genomic analysis, particularly the development of genome-wide association studies, have facilitated the identification of genomic risk factors for DILI, but, to date, there are only two main examples, liver injury caused by amoxicillin-clavulanate (AC) and by flucloxacillin, where genetic risk factors causing the injury have been identified and replicated with understanding of the underlying mechanism.

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