Interplay Among Nitric Oxide and Reactive Oxygen Species A Complex Network Determining Cell Survival or Death

Programmed cell death (PCD) is an integrated cellular process occurring in plant growth, development, and defense responses to facilitate normal growth and development and better survival against various stresses as a whole. As universal toxic chemicals in plant and animal cells, reactive oxygen or nitrogen species (ROS or RNS), mainly superoxide anion (O-2(-center dot)), hydrogen peroxide (H2O2) or nitric oxide ((NO)-N-center dot), have been studied extensively for their roles in PCD induction. Physiological and genetic studies have convincingly shown their essential roles. However, the details and mechanisms by which ROS and (NO)-N-center dot interplay and induce PCD are not well understood. Our recent study on Cupressus lusitanica culture cell death revealed the elicitor-induced co-accumulation of ROS and (NO)-N-center dot and interactions between (NO)-N-center dot and H2O2 or O-2(-center dot) in different ways to regulate cell death. (NO)-N-center dot and H2O2 reciprocally enhanced the production of each other whereas (NO)-N-center dot and O-2(-center dot) showed reciprocal suppression on each other's production. It was the interaction between (NO)-N-center dot and O-2(-center dot) but not between (NO)-N-center dot and H2O2 that induced PCD, probably through peroxynitrite (ONOO-). In this addendum, some unsolved issues in the study were discussed based on recent studies on the complex network of ROS and (NO)-N-center dot leading to PCD in animals and plants.