Nitric oxide protects against cellular damage produced by methylviologen herbicides in potato plants.

Methylviologen compounds are normally used in agronomy as herbicides. They cause an overproduction of reactive oxygen species (ROS) within chloroplasts, subjecting the plant to a severe oxidative stress. Since nitric oxide (NO) is a bioactive ROS scavenger, we analyzed its effect over some toxic processes caused by the methylviologens diquat and paraquat in potato leaves (Solanum tuberosum L. cv. Pampeana). Three NO donors, (i) sodium nitroprusside (SNP), (ii) S-nitroso-N-acetylpenicillamine, and (iii) a mixed solution of ascorbic acid and NaNO2, were able to prevent chlorophyll loss. Residual products from NO generation and decomposition failed to prevent chlorophyll decline and a specific NO scavenger, carboxy-PTIO, arrested NO-mediated chlorophyll protection. Dichlorophenyldimethylurea, an inhibitor of chloroplastic electron transport, mimicked NO-mediated chlorophyll protection. During oxidative stress, cell ion leakage to intercellular compartments occurs as an early step, leading to a special kind of programmed cell death. NO proved to specifically decrease the extent of ion leakage originated by diquat, since the protection originated by 100 microM SNP was completely arrested by carboxy-PTIO. These results suggest that NO can strongly protect plants from methylviologen damage and strengthen the evidence in favor of NO as a potent antioxidant in some situations.