Figure 2
From: Oxidative stress mediates end-organ damage in a novel model of acetaminophen-toxicity in Drosophila
APAP induces ROS, depletes glutathione, and requires Cyp18a1 bioconversion for toxicity in Drosophila fat body. Representative fluorescent images of fat body of early third instar Drosophila larvae after 4 h of feeding the ROS sensitive dye HydroCy3 and either (A) PBS or (B) 100 mM APAP in PBS. (C) Quantification of fluorescence intensity from imaged fat bodies. *p < 0.05 as determined by t-test. n = 13 larvae per condition. (D) Total glutathione content of whole Drosophila treated with either vehicle control or 100 mM APAP for 3 days. ****p < 0.0001 as determined by t-test; n = 3. (E) Redox potential of whole Drosophila after 3 days of treatment with either vehicle control or 100 mM APAP for 3 days. ***p < 0.001 as determined by t-test; n = 3 (F) Schematic of APAP metabolism and mechanism of toxicity. (G) Effect of fat body-specific depletion of CYP18A1 on survival of Drosophila treated with 50 mM APAP. Log-Rank test p < 0.0001, n = 60. (H) Measurement of native acetaminophen from whole flies using mass spectrometry, n = 1.
