Macrophage Nrf2 confers resistance to oxidative stress. (A and B) DNA oxidation (8oxodG, red, A) and ARE-GFP activation (green, GstD1, ARE-GFP reporter, B) increased as embryonic macrophages matured. (C) ROS levels (DHE, magenta) increased in stage 15 srp > Nrf2^RNAi macrophages. (D and E) stage 15 srp > Nrf2^RNAi macrophages accumulated oxidative damage (8oxodG, D and D′) and DNA damage (H2AvD, E and E′). (F) The H99 mutation rescued the accumulation of DNA oxidative damage (8-oxodG) caused by corpse uptake and exacerbated by down-regulation of Nrf2. (G) Schematic of Nrf2 activation within macrophages. In all figures, the cell body is indicated by a dashed white outline. Macrophages labeled in green (srp > GFP, A, C, and F) or red (anti-fascin, B and E) srp > GFP, D). Adjacent epithelium is marked by yellow dashed lines (D, E, and F). Data (C, D, E, and F) were generated using Nrf2^RNAi Flybase ID FBtp0069370. ns: not significant, **P < 0.01, ****P < 0.0001 via Mann–Whitney test (A′, B′, C′, D′, E′) or one-way ANOVA followed by Krushal–Wallis comparison analysis (F′). Images were collected from: 9 stage 12, 10 stage 13, 10 stage 15 embryos (A); 8 stage 12, 10 stage 15 embryos (B); 11 control and 17 srp > Nrf2^RNAi embryos (C); 28 control and 29 srp > Nrf2^RNAi embryos (D); 9 control and 10 srp > Nrf2^RNAi embryos (E); 5 control, 5 Nrf2^RNAi and 7 Nrf2^RNAi; H99 embryos (F).