Figure 2.

Non-cytotoxic levels of oxidative stress induce mitochondrial DNA depletion, impair cellular bioenergetics and stimulate inflammation. BEAS2B cells were treated with several concentrations of GOx for 1 h and immediately post-challenge as well as 24 h later were measured: (A) mitochondrial DNA integrity, (B) mitochondrial DNA content, (C) apoptotic/necrotic cell death; (D) mitochondrial respiration; (E) glycolysis. (F) 3-D reconstruction of cellular morphology of BEAS2B at 24 h after GOx-treatment was visualized using ATPA-specific antibody (green), β-tubulin (red) and nucleus (DAPI, blue). (G) Amount of pro-inflammatory mediators in medium of BEAS2B cells measured at 24 h post GOx-treatment. Data represent average ± SEM of n = 5 biological replicates. (H) Lack of enhanced production of IL-6 in BEAS 2B cells stimulated with inactive GOx at 24 h. Representative data of n = 3 independent experiments are shown. *p < 0.05, **p < 0.01 vs. control.