Figure 1.

Writer deficient mouse livers have increased sensitivity to APAP induced stress and display decreased selenoprotein levels. (A) APAP can be converted into a non-toxic form by UDP-glucuronosyltransferases (UGT) or a toxic form by cytochrome P450 enzyme (CYP2E1) to generate the reactive intermediate metabolite N-actyl-p-benzoquinone imine (NAPQI). Male C57Bl/6 WT (blue) and Alkbh8^Def (red) mice (8–12 weeks old) were exposed to a single dose of APAP (B–D) or daily dose of APAP over 4 days (E–G), and tissue/blood was harvested. (B,E) ALT and (C,F) 8-isoprostane levels were determined in blood and liver samples, respectively for WT saline (blue circle), Alkbh8^Def saline (red square), WT APAP (blue triangle) and Alkbh8^Def APAP (red triangle) (D,G) Gpx3 protein levels in the liver were evaluated using the ProteinSimple WES system. Statistical significance (N = 3) was measured by an unpaired t-test with (* p < 0.05, ** p < 0.01, and *** p < 0.001).