The Chemical Interplay between Nitric Oxide and Mitochondrial Cytochrome c Oxidase: Reactions, Effectors and Pathophysiology
Figure 3
Melatonin-induced changes of the nNOS mRNA expression in HaCaT cells: effect on NOx production and mitochondrial membrane potential. (a)—Real-time PCR quantification of nNOS mRNA (β-actin gene used for normalization). (b)—Fluorometric determination of the NOx release in the cell culture medium. (c)—Mitochondrial membrane potential evaluated as the fluorescence difference, F, from the maximal (plateau) to the minimal level reached after addition of valinomycin (see also Figure 2(c)). (d)—Contribution of oxidative phosphorylation and glycolysis to ATP production, directly evaluated according to [47]. The ATPglycolytic/ATPOXPHOS ratio is indicative of the ability of a given cell line to compensate with glycolysis an OXPHOS impairment (so-called, Warburg effect) [48, 49]. The release of NO induced by melatonin almost doubles the glycolytic contribution to ATP synthesis in HaCaT cells. Cells were incubated with 1 nM melatonin for 6 h. (a), (b): ** versus CTR; (c), (d): * versus CTR. Modified from [48].
