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. Author manuscript; available in PMC: 2015 Feb 17.
Published in final edited form as: Free Radic Biol Med. 2009 Jun 12;47(6):750–759. doi: 10.1016/j.freeradbiomed.2009.06.010

Figure 5. Mitochondrial hOggl prevents oxidant-induced toxicity independent of its 8-oxoG DNA repair activity.

Figure 5

Transient overexpression of empty vector control, wild-type mt-hOgg-1 as well as two previously described hOgg-1 mutant plasmid constructs lacking 8-oxoguanine DNA repair capacity (317–323 long alpha/beta and V317) were done by lipofectamine as described in the Methods (18). Mitochondrial localization was confirmed by C-Myc immunostaining. Similar to wild-type mt-hOgg-1, overexpression of mt-hOgg-1 mutants 317–323 long alpha/beta or V317 completely blocked oxidant induced caspase-9 activation (A), DNA fragmentation (B), and the decrease in mitochondrial aconitase activity (C) caused by H2O2 (100 µM) or asbestos (25 µg/cm2) for 24h. * p < .05 v. no H2O2 or asbestos; † p < .05 v. empty vector cells exposed to the same dose of 2O2 or asbestos.