Abstract
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 (O2-•), hydrogen peroxide (H2O2) or nitric oxide (•NO), have been studied extensively for their roles in PCD induction. Physiological and genetic studies have convincingly confirmed their essential roles. However, the details and mechanisms by which ROS and •NO interplay and induce PCD are not understood. Our study on cell death in elicitor-treated Cupressus lusitanica cell culture revealed the elicitor-induced co-accumulation of ROS and •NO and interactions between H2O2 or O2-• with •NO in different ways to regulate cell death. •NO and H2O2 reciprocally enhanced on production of each other whereas •NO and O2-• showed reciprocal suppression on each other’s production. It was •NO and O2-• interaction but not •NO and H2O2 interaction that induced PCD, probably through peroxynitrite (ONOO-). In this addendum, some unsolved issues in the study were discussed on the basis of recent studies of the complex network of ROS and •NO leading to PCD in animals and plants.
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