Redox-Regulation of S-nitrosoglutathione reductase – ROS-mediated inhibition of GSNOR contributes to the activation of anti-oxidative mechanisms

We demonstrated that GSNOR activity can be inhibited in-vitro by H2O2, as well as in-vivo by paraquat, which is accompanied by a significant change in NO homeostasis. The observed increase in cellular SNOs consequently leads to induction of NO-dependent signaling mechanisms, resulting in GSH accumulation, enhanced activity of GSH-related enzymes and finally in a protection against oxidative stress. All these findings substantiate the physiological importance of GSNOR in fine-tuning the levels of NO/SNO during plant growth and development and also in many stress response reactions. Moreover, ROS-dependent inhibition of GSNOR is playing an important role in activation of anti-oxidative mechanisms to damping oxidative damage and implies a direct crosstalk between ROS- and NO-signaling.

Christian Lindermayr

Model illustrating the function of GSNOR in oxidative stress. Abiotic or biotic stressors induce accumulation of ROS (oxidative burst), which inhibits the activity of GSNOR and results in accumulation of GSNO/SNOs. The enhanced levels of SNOs induce the biosynthesis of GSH and enhance the activity of GSH-dependent enzymes which counteract an accumulation of ROS. Black and red lines indicate stimulating or inhibiting effects, respectively. GSNO(R), S-nitrosoglutathione-(reductase); SNO, S-nitrosothiols; GSH, glutathione; GR, glutathione-reductase; GST, glutathione-S-transferase.
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