Nitric oxide, induced by wounding, mediates redox regulation in pelargonium leaves.

The subject of this study was the participation of nitric oxide (NO) in plant responses to wounding, promoted by nicking of pelargonium (Pelargonium peltatum L.) leaves. Bio-imaging with the fluorochrome 4,5-diaminofluorescein diacetate (DAF-2DA) and electrochemical in situ measurement of NO showed early (within minutes) and transient (2 h) NO generation after wounding restricted to the site of injury. In order to clarify the functional role of NO in relation to modulation of the redox balance during wounding, a pharmacological approach was used. A positive correlation was found between NO generation and regulation of the redox state. NO caused a slight restriction of post-wounded O(2) (-) production, in contrast to the periodic and marked increase in H(2)O(2) level. The observed changes were accompanied by time-dependent inhibition of catalase (CAT) and ascorbate peroxidase (APX) activity. The effect was specific to NO, since the NO scavenger 2-(4-carboxyphenyl)-4,4,5,5 tetramethylimidazoline-1-oxyl-3-oxide (cPTIO) reversed the inhibition of CAT and APX, as well as temporarily enhancing H(2)O(2) synthesis. Finally, cooperation of NO/H(2)O(2) restricted the depletion of the low-molecular weight antioxidant pool (i.e. ascorbic acid and thiols) was positively correlated with sealing and reconstruction changes in injured pelargonium leaves (i.e. lignin formation and callose deposition). The above results clearly suggest that NO may promote restoration of wounded tissue through stabilisation of the cell redox state and stimulation of the wound scarring processes.