The Role of Mitochondrial Reactive Oxygen Species in Cardiovascular Injury and Protective Strategies

Table 2

Potential mechanisms responsible for the decrease in ROS generation.

Site of action	Mechanism
() UCP2 or UCP3 overexpression [131–133]	Reduced mitochondrial ROS production via mitochondrial uncoupling with subsequent depolarization
() Brief transient mPTP opening [134]	Reduced ROS production and/or release into the cytosol via a reversible depolarization; Observation: a prolonged mPTP opening triggers apoptosis and cell death [135, 136]
() Recruitment of hexokinase (HK) at the mitochondrial outer membrane [137]	Increased coupled respiration with subsequent reduced electron leak and ROS production
() Glutathionylation of CII and CV [92, 138, 139]	Decreased activity of CII and CV
() Glutathionylation of the 51-kDa (NDUFV1) and 75-kDa (NDUFS1) CI subunits [79, 81, 140, 141]	Decreased activity of CI; Observation: however, CI inactivation is not necessarily linked to reduced ROS production since Taylor and collaborators demonstrated that glutathionylation of CI was associated to increased superoxide production [142]
() Reduction of electrons input [143, 144]	Lowered cellular glucose uptake and stimulation of pyruvate conversion to lactate with secretion of the latter into the extracellular environment
() Mild uncoupling [145, 146] and inhibition of succinate dehydrogenase [147] via the action of potassium channel openers	Inhibition of CI with subsequent reduction of H2O2 release into the cytosol