Skip to main content
. Author manuscript; available in PMC: 2011 Apr 19.
Published in final edited form as: Chem Res Toxicol. 2010 Apr 19;23(4):778–787. doi: 10.1021/tx900415k

Figure 2.

Figure 2

Measurement of NO synthesis, NO consumption, and O2 consumption by bone marrow-derived macrophages (BMDM) and RAW264.7 cells. Shown are NO concentrations (black) and O2 concentrations (gray) as a function of time for representative closed-chamber experiments. The linear decline in O2 concentration in the absence of NO for unactivated macrophages (8 × 106 cells) indicates that the rate of O2 consumption is constant. Measurements with unactivated RAW264.7 and HCT116 cells resulted in similar plots (not shown). NO and O2 concentrations were also measured for 8 × 106 BMDM after activation by 12 h exposure to IFN-γ and LPS. The rate of O2 consumption slowed as the NO concentration increased. The kinetics of NO synthesis and consumption are reflected in the plateau concentration for NO and the rate at which the plateau is reached. Plots of NO and O2 concentrations measured for activated RAW264.7 cells were nearly identical (not shown). O2 concentrations are also depicted for activated RAW264.7 cells after 1 h exposure to rotenone, a respiratory inhibitor; the reduced slope corresponds to about an 85% reduction in the overall rate of O2 consumption.