Nitric oxide preserves the level of chlorophyll in potato leaves infected by Phytophthora infestans

Nitric oxide (NO) is a bioactive molecule involved in many physiological processes. Among its biological function, NO has been proved to be cytotoxic against microorganisms in cells of the immune response, thus preventing infection. We have specifically studied the effect of a NO donor, sodium nitroprusside (SNP), on the chlorophyll content in potato leaves infected with the pathogenic fungus Phytophthora infestans (Pi). Fifteen days after infection, chlorophyll content strongly decayed in water-treated potato leaf sections. SNP was able to partially revert that loss in a dose-dependent manner, being the effective SNP concentrations between 10 μM and 100 μM. NaNO2 and NaNO3, the SNP-dedved residual products, were unable to prevent the chlorophyll loss. Treatments with SNP did not affect the survival of Pi and the fungus was able to grow in a V8-agar medium containing 100 μM SNP. Both the amount and the extent of germination of Pi sporangia resulted similar in the absence and in the presence of SNP. Respiratory inhibitors of the cyanide-sensitive and cyanide-resistant pathways, 2,4-dinitrophenol and salicylhydroxamic acid respectively, did not change the chlorophyll levels in infected potato leaves, suggesting that NO effect should not be on mitochondrial respiration. These results indicate that NO could be a protective molecule, either preserving the chloroplast membrane of infected leaf sections against the toxicity of reactive oxygen species or being directly involved in any step of the chlorophyll metabolic pathway.