(λex = 488 nm, λem = 575-650 nm) as well as weak fluorescence in Channel 4 (λex = 514 nm, λem = 520-575 nm). The two fluorescence channels affected by SIN-1 were then evaluated using the ONOO -scavenger, uric acid. The addition of uric acid (500 μM) and SIN-1 (1.0 mM) led to a 0.35-fold decrease in the average green fluorescence intensity and 1.83-fold enhancement in the average red fluorescence intensity, when compared with the corresponding SIN-1 group (green and red channels, respectively, Fig. ). These results indicate that an increase of ONOO -can result in depletion of ATP, which is in agreement with previous studies. We then set out to evaluate how imbalances in the energy metabolism instigated by obstructing ATP production can influence production of ONOO -. Oligomycin A inhibits ATP synthase by blocking its FO unit. As shown in Fig. , after the hepatocytes were incubated with oligomycin A (25 μM) for 1 h, the intensities obtained from imaging in the red channel revealed a significant decrease (35% of the initial level, Fig. ), and 1.55-fold increase in the green channel suggestive of an increase in level of ONOO -when compared with healthy hepatocytes (Fig. ). Next, following the addition of exogenous ATP (10 mM), the intensity of green channel is 85% of the control group (Fig. ) and the intensity from the red channel increased to almost the same level as the control group (Fig. ), which indicated that the addition of ATP induced recovery. These results indicated production of ROS/RNS is affected by mitochondrial damage to ATP synthesis, leading to an increase of ONOO -. While this influence could be diminished by the addition of ATP. Which confirms that the inhibition of ATP synthase results in the production of ONOO -.