Mitochondria generate cellular energy through TCAcycle and electron transport chain. ETC is located in the inner mitochondrialmembrane. The products of TCA cycle ie the reducing equivalents (NADH and FADH2)are reoxidized via the transfer of electrons through the electron transportchain (ETC). NADH donates electrons tocomplex I (NADH-ubiquinone oxidoreductase)) of the ETC and FADH2 to complex II ( succinate-ubiquinoneoxidoreductase ).

ComplexI and II then transfer the electrons to ubiquinone Ubiquinone passes itselectrons to complex III (Ubiquinol-cytochrome c oxidoreductase), cytochrome C, complex IV (Cytochrome c oxidase), and finally to molecular oxygen. As the electronsare transferred through the ETC the energy is used to shuttle protons acrossthe membrane. This creates a voltage across the inner and outer membrane of themitochondria and drives ATP synthesis.

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Translocation ofprotons across the mitochondrial inner membrane, thereby creating thetransmembrane electrochemical gradient (150–200 mV negative to the cytosol). Theelectrochemical potential make ATP from ADP and Pi, mediated byproton movement back through the ATP synthase complex. Under normal conditions,the proton gradient is also diminished by H+ ‘leak’ to the matrix.The ‘leak’ occurs either via non-protein membrane pores, protein–lipidinterfaces (H+ leak), or by proton channels known as uncouplingproteins (UCPs).

In hyperglycemic conditions,the number of substrates entering the TCA cycle is greatly increased and consequentlythe number of reducing equivalents donating electrons to the ETC is also increased.Once the ETC reaches a threshold voltage across the membrane the electrons beginto back up at complex III. These electrons are then donated to molecularoxygen, which in turn results in an increase in mitochondrial superoxideproduction (Brownlee, 2001). Themitochondrial isoform of superoxide dismutase degrades oxygen free radical tohydrogen peroxide, which is later converted to H2O and O2 by other enzymes.Thusmitochondria initiates hyperglycemia-induced superoxide production, this, inturn, can activate a number of other superoxide production pathways which mayamplify the original damaging effect of hyperglycemia (Ferdinando and Michael, 2010). These pathways include redox changes, NADPH oxidases, anduncoupled eNOS .