The Trx and GSH redox systems limit oxidative/nitrosative stress caused by ROS/RNS and function via Trx reductase and GSH reductase enzyme activities. NO may directly cause increased RNS production (via peroxynitrite formation) although NO may also interact with GSH leading to GSNO formation through S-nitrosylation. GSNOR is the major enzyme involved in GSNO metabolism and protects against increased ROS/RNS. (GSSG, glutathione disulfide; S-nitroso-GSH, GSNO; ROS, reactive oxygen species; RNS, reactive nitrogen species; NO, nitric oxide)