Figure 5
From: Oxidative stress mediates end-organ damage in a novel model of acetaminophen-toxicity in Drosophila
Genetic and pharmacologic modification of antioxidant response pathways alter APAP toxicity in Drosophila. (A) Schematic representation of glutathione generation in metazoans, highlighting the role of Nrf2/CncC, N-acetylcystein, and methione (in yellow). (B) Representative images and (C) quantification of mean GFP fluorescence in control and 100 mM APAP treated ARE-GST-GFP animals. (D) Survival of vehicle treated and 50 mM APAP-treated control and experimental animals, in which dNrf2 knockout (cnccIR) is depleted in the Drosophila fat body using the fat body driver Yolk-Gal4. Log-Rank test p < 0.0001, n = 60. (E) Effect of 100 mM N-acetylcysteine supplementation on APAP toxicity. (F) Effect of 10 mM Methionine supplementation of APAP toxicity. Log-Rank test p < 0.0001, n = 60.
