the dual role of snitrosoglutathione gsno during thymocyte apoptosis nitric oxide no is known to regulate redoxsensitive signalling pathways in physiology and pathophysiology depending on its concentration the noreleasing compound snitrosoglutathione gsno causes negative and positive regulation of thymocyte apoptosis at levels below 06 mm gsno produces deoxyribonucleic acid dna laddering which is inhibited by activation of protein kinase c pkc cycloheximide treatment and calcium chelation higher concentrations of the no donor 12 mm suppress thymocyte apoptosis initiated by the classical agonist dexamethasone inhibition of apoptosis by no is analogous to the action of the thiolblocking compound nethylmaleimide nem and the glutathionestransferase substrate 1chloro24dinitrobenzene cdnb inhibition of apoptosis results from thiol modification of critical proteins in response to no treatment depending on the concentration gsno can be involved either in toxic or in protective signalling in thymocyte biology