Figure 6.

Model of UCP2 function in resting thymocytes (see Discussion for details). Protons are pumped into the mitochondrial intermembrane space by complexes of the electron transport chain during oxidation of substrates. UCP2 mediates a significant portion of mitochondrial proton leak in resting thymocytes, thus providing one of three possible routes for protons to re-enter the matrix (the other two being ATP synthase and UCP2-independent leak). UCP2 deficiency causes an increase in ΔΨ_m. This increase may either put backpressure on the proton pumps in the electron-transport chain (1), thus inhibiting substrate oxidation and oxygen consumption rates, or increase ATP production (2).