Figure 3 | Scientific Reports

Figure 3

From: Loss of the Mitochondrial Fatty Acid β-Oxidation Protein Medium-Chain Acyl-Coenzyme A Dehydrogenase Disrupts Oxidative Phosphorylation Protein Complex Stability and Function

Figure 3

143B MCAD knockout (KO) cells exhibit defects in mitochondrial respiration and are more sensitive to OXPHOS inhibitor-induced oxidative stress. (A) Mitochondrial oxygen consumption in MCAD knockout (KO) cells was not significantly different to control (CON) cells in the presence of glucose. However, oxygen consumption was significantly lower in MCAD KO cells in the presence of galactose. Data is mean ± s.d., n = 3. *p < 0.05. Mitochondrial reactive oxygen species generation was assessed in live cells using the superoxide probe MitoSOXTM. There was no difference in mitochondrial superoxide generation between CON and MCAD KO cells over a 60 min time course in either untreated conditions (B) or with the addition of the OXPHOS complex I inhibitor rotenone (C). (D) Mitochondrial superoxide generation was significantly greater in MCAD KO cells compared to CON cells after 30 min (p = 0.001), 45 min (p = 0.0005) and 60 min (p = 0.0034) in the presence of the OXPHOS complex III inhibitor antimycin A. Data is mean ± s.d., n = 5.

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