TBI induces mitochondrial fission and oxidative stress in the intestinal epithelium. The small bowel of BALB/c mice treated with TBI was resected at the indicated time points and evaluated for changes in mitochondrial architecture. (A) Representative electron micrograph for each time point is shown. (B-C) Enriched mitochondrial fractions isolated 24 hours after TBI from the small bowel of mice. (B) A representative western blot probed with antibodies against dynamin-related protein 1 (DRP1) for mitochondrial fission, and VDAC-1 for total mitochondrial content (left) and densitometric protein quantification (n = 3; right) is shown. (C) A representative western blot derivatized with dinitrophenylhydrazine (DNP) and probed with antibodies against DNP for protein carbonylation and VDAC-1 for total mitochondrial content (left) and densitometric protein quantification (n = 3; right) is shown. CT, control (nonirradiated) mice; ∗P < .05, and ∗∗P < .01; n, number of mice). VDAC-1, Voltage-dependent anion-selective channel 1.