Journal Article10.1152/AJPCELL.1991.260.5.C910
Effect of exogenous and endogenous nitric oxide on mitochondrial respiration of rat hepatocytes.
409
TL;DR: Endogenous .N = O biosynthesis was induced in HC by a specific combination of cytokines and lipopolysaccharide, and a concentration-dependent inhibition of mitochondrial aconitase, NADH-ubiquinone oxidoreductase, and succinate-ubsinone oxidation chain was observed.
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Abstract: Although nitric oxide (N = O) biosynthesis is inducible in rat hepatocytes (HC), the physiological significance of N = O production by these cells is unknown Short exposure of HC to authentic N = O led to a concentration-dependent inhibition of mitochondrial aconitase, NADH-ubiquinone oxidoreductase, and succinate-ubiquinone oxidoreductase (complexes I and II of the mitochondrial electron transport chain) Most susceptible to N = O inhibition was mitochondrial aconitase, in which a reduction in enzyme activity to 202 +/- 16% of control was observed In contrast to mitochondrial aconitase, cytosolic aconitase activity was not inhibited by N = O After exposure to a maximal inhibitory concentration of N = O, mitochondrial aconitase activity recovered completely within 6 h Complex I did not fully recover within this incubation period Endogenous N = O biosynthesis was induced in HC by a specific combination of cytokines and lipopolysaccharide After 18 h of incubation with these stimuli, a significant inhibition of mitochondrial aconitase activity to 708 +/- 24% of controls was detected However, this was due only in part to the action of N = O A non- N = O-dependent inhibition of mitochondrial function appeared to be mediated by tumor necrosis factor
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Macrophage oxidation of l-arginine to nitrite and nitrate
Michael A. Marletta
- 01 Jan 1988
TL;DR: L-Arginine is required for the activation of macrophages to the bactericidal/tumoricidal state and suggests that nitric oxide is serving as an intracellular signal for this activation process in a manner similar to that very recently observed in endothelial cells, where nitrics oxide leads to vascular smooth muscle relaxation.