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. Author manuscript; available in PMC: 2016 Jun 2.
Published in final edited form as: Free Radic Biol Med. 2015 Jul 21;89:379–386. doi: 10.1016/j.freeradbiomed.2015.07.017

Figure 4. Absence of MnSOD expression results in increased mitochondrial oxidative stress and alters mitochondrial electron transport chain function.

Figure 4

(A) An increase in mean fluorescent intensity (MFI) of dihydroethidium (DHE) and MitoSOX red staining was detected by flow cytometry in SOD2 knock-out cells (open bars) compared to wild-type cells (closed bars). *P = 0.012 compared to wild-type.

(B) Activities of complex I (left panel) and complex II (right panel) (µmol/min/mg protein) were measured spectrophotometrically. Complex I activity was measured as the rate of rotenone-inhibitable NADH oxidation in the presence or absence of rotenone. Complex II was assayed as the rate of DCIP reduction by Coenzyme Q in the presence and absence of succinate. Activity measurements were normalized to total cellular protein. *P<.05 compared to wild-type.

(C) Increased succinate dehydrogenase activity was detected by histochemical staining in wild-type cells (left panel) compared to knock-out cells (right panel)

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