Nitric Oxide and the Liver

The pathological response to nitric oxide (NO) will vary in relation to the context in which NO is produced, duration, level of radical oxygen species generated and the amount of antioxidants present within the environment. The effect of NO on the primary liver cell type, hepatocytes, is controlled by the NO downstream activation of soluble guanylate cyclase and cyclic guanosine monophosphate, protein complex assembly, overexpression of stress-induced proteins or protein modification of the active site of caspase(s) by the S-nitrosative modification of cysteine. The pathophysiological roles of NO in liver will be presented with special attention of the use of experimental data generated through the use of pharmacological NO donors, inhibitors to NO generation, modulation of inflammatory cytokines, cofactor, or substrate within genetically altered knockout animals or patients when applicable.