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. 2016 Mar 4;11(3):e0150459. doi: 10.1371/journal.pone.0150459

Fig 8. Schematic representation of mitochondrial dysfunction modulation by NO2-AA in a cellular model of kidney cells activated by ANG II.

Fig 8

On the left of the diagram, the stimulation with ANG II in HK-2 increases the O2.- production as well as inducible NOS expression and formation of peroxynitrite. This highly oxidizing molecule produces a decrease in the activities (red line) of the respiratory chain complex SDH (complex II) and ATPase (complex V) as well as increases oxidation and nitration of mitochondrial proteins. Therefore, HK-2 exposed to ANG II exhibited mitochondrial dysfunction. The right side of the diagram represent the modulation of cell damage by the nitroalkene. In the presence of NO2-AA a reduction of ANG II-induced HK-2 damage is produced, with lower extents of O2.- production as well as lower levels of inducible NOS expression leading to a decrease in peroxynitrite formation. The activities of the respiratory chain complex are restored and NO2-AA also prevents oxidation and nitration of mitochondrial proteins. In summary, NO2-AA modulates ANG II mediated oxidative damage improving mitochondrial function.