Table 3.

Effect of mitochondrial morphology regulation on mitochondrial ROS production

Manipulation/Condition	Cell Type	Effect on Mitochondrial ROS Production	Reference
Pro-fusion (elongation)
DRP1K38A overexpression	Clone 9 hepatocytes	Prevented 1- to 1-fold increase in ROS [DHE] during hyperglycemia	162
MFN2 overexpression	H9c2 myoblasts	Prevented 1.5-fold increase in ROS [DHE] during hyperglycemia	162
MFN2 overexpression	H9c2 myoblasts, endothelial cells, smooth muscle cells	Prevented 50% increase in ROS [DHE] during hyperglycemia	163
DRP1 RNAi	Endothelial cells	Prevented 3-fold increase in ROS [MitoSOX] and further reduced ROS by 60–70% during hyperglycemia	129
Fis1 RNAi	Endothelial cells	Prevented 3-fold increase in ROS [MitoSOX] during hyperglycemia	129
DRP1 inhibition (Mdivi-1)	C2C12 myoblasts	Prevented 15–20% increase in ROS [H2DCFDA] with palmitate	76
Pro-fission (fragmentation)
Hyperglycemia	Endothelial cells, myoblasts, hepatocytes	Increases ROS 1- to 3-fold, which can be prevented by blocking fission (see above)
Mechanical isolation of mitochondria	Myofibers	Increased total ROS 5- to 10-fold [Amplex Red], and free radical leak 9- to 23-fold (per unit O2 consumed)	115

ROS, reactive oxygen species; DHE, dihydroethidium is a superoxide probe; H₂DCFDA, carboxy-dichlorodihydrofluorescein is a broad-scope ROS probe; MitoSox is a mitochondria-targeted superoxide probe; Amplex Red is a H₂O₂ probe.