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. 2011 May 12;286(26):22846–22854. doi: 10.1074/jbc.M111.231902

FIGURE 6.

FIGURE 6.

Iron bioavailability and restoration of mitochondrial aconitase activity after DETA/NO removal in wild-type versus IRP1-deficient BMMs. A, wild-type and IRP1-null BMMs were exposed to 250 μm DETA/NO for 18 h. NO was then removed by extensive washing (time 0), and cells were further incubated in fresh medium for up to 2 h. Crude mitochondrial extracts were collected 0, 0.5, 1, and 2 h after NO removal to analyze the recovery of mitochondrial aconitase activity. B, mitochondrial aconitase activity in wild-type versus IRP1-null BMMs expressed as a percentage of control, i.e. wild-type and IRP1-null cells incubated in DETA/NO-free medium during the first 18 h but otherwise processed in an identical manner. Data are presented as mean ± S.D., n = 5. C, Western blot analysis of mitochondrial aconitase levels in crude mitochondrial extracts. Representative immunoblots are shown. The succinate dehydrogenase, subunit A complex II subunit was used as a loading control. The histograms show mitochondrial aconitase levels (mean ± S.D., n = 4) as a percentage of control (no DETA/NO) cells after normalization to succinate dehydrogenase, subunit A. *, p < 0.05, Student's t test.