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. Author manuscript; available in PMC: 2015 Sep 1.
Published in final edited form as: Free Radic Biol Med. 2014 Jul 1;0:157–174. doi: 10.1016/j.freeradbiomed.2014.06.006

Figure 10.

Figure 10

Dox (also called adriamycin, ADR) induces nitrosative stress in brain mitochondria. WT mice were injected i.p. with Dox. (A). i-NOS message was induced, but anti-TNFα antibody prevents i-NOS induction following ADR treatment. (B). The RCR, a measure of oxygen consumption, in brain mitochondria isolated from ADR-treated WT mice is significantly depressed, but not in i-NOS knock-out mice. (C). Mitochondrial-resident MnSOD is nitrated following ADR addition to WT mice, but not in i-NOS knock-out mice. (D). MnSOD activity is significantly depressed in mitochondria isolated from brain of ADR-treated WT mice, but not in i-NOS knock-out mice. (E). Mitochondria isolated from brain of ADR-treated WT mice lead to cytochrome c release, but not in mice also treated with anti-TNFα antibody. Note that ADR-treated WT mice also treated with IgG still lead to cytochrome c release from mitochondria isolated from brain, suggesting specificity of the anti-TNFα treatment. (F). Consistent with the results of (E), apoptosis occurs in brain of ADR-treated WT mice as assessed by TUNEL staining even at 3h post-ADR treatment, and pronounced apoptosis at 72h post-ADR treatment occurred. This latter time is the time at which oxidative stress in brain is maximal. The figure, used with permission from Elsevier Science Publishers, was modified from reference [171].