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. 2016 Nov 16;312(2):F266–F275. doi: 10.1152/ajprenal.00473.2016

Fig. 2.

Fig. 2.

Hyperglycemic switch from mitochondrial NO to superoxide production. A: human umbilical vein endothelial cells (HUVEC) respond to the calcium ionophore (A-23187) with an increase in mitochondrial NO production, as detected using diacetate (4-amino-5-methylamino-2′,7′-difluorofuorescein (DAF) fluorescence (after selective loading of DAF in mitochondria). This process is inhibited by elevated ambient d-glucose (but not l-glucose) level. B: pretreatment of HUVEC with a cell-permeable superoxide dismutase (SOD) mimetic, manganese (III) tetrakis (4-benzoic acid)porphyrin chloride (Mn-TBAP), protects mitochondrial NO production against impairment by high d-glucose. C: eNOS expression in mitochondrial fractions (mt) or whole cell lysates (cell) is not affected by high levels of ambient d-glucose. Cytochrome c oxidase (COX) was used as a mitochondrial marker. D: NO production by mitochondria isolated from the livers of Zucker diabetic fat (ZDF) or Zucker lean (ZL) rats. Note that NO generation by mitochondria of ZDF rats is impaired under basal and stimulated conditions (*P < 0.05).