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Teschke R, Uetrecht J (2021) Mechanism of idiosyncratic drug induced liver injury (DILI): Unresolved basic issues

Activity was quantified using the Ransod kit (Randox Laboratories, United Kingdom), measuring inhibition of superoxide radical-mediated reduction of nitroblue tetrazolium (NBT) to formazan at 560 nm (DU65 spectrophotometer, Beckman, Germany)

Ruvolo P, Qiu Y, Ruvolo V, Wang RY, Zeng Z, Burks J, Pan R, Hail Jr N, McQueen T, Yoo SY, Kornblau SM, and Andreeff M

Its key feature lies in the competitive utilization of the same substrate by iNOS (also known as Nos2) and Arg1: the former generates NO and is closely associated with pro-inflammatory effects, whereas the latter produces ornithine and polyamines and participates in tissue repair and immune regulation ( Under classical pro-inflammatory stimulation (such as LPS/IFN-), iNOS expression is upregulated and catalyzes the conversion of Arg into NO and citrulline

Valpha14iNKT cell deficiency prevents acetaminophen-induced acute liver failure by enhancing hepatic glutathione and altering APAP metabolism

N-acetyl cysteine overdose inducing hepatic steatosis and systemic inflammation in both Propacetamol-induced hepatotoxic and Normal mice