Diamide or PMA induced enhanced oxidative stress attenuate basal as well as LPS/cytokines induced iNOS/NO generation.
High ROS in PMNs of CML subjects linked with reduced iNOS/NO, and were unresponsive to LPS/cytokines mediated induction.
S-Glutathionylation of NFκB under excessive ROS limits its binding to iNOS promoter.
DTT reverses NFκB S-glutathionylation, improves DNA binding activity and enhanced iNOS expression/NO generation.
Enhanced NOX2, mitochondrial ROS and reduced GSH/Grxs regulate NFκB S-glutathionylation in CML.