Nitric oxide functions as a potent antioxidant against methylviologen-mediated damage to lipids, proteins and RNA in plants.

BELIGNI, MV; LAMATTINA, L

Conferencia; Biology, Chemistry and Therapeutic Applications of Nitric Oxide: First International Conference; 2000

Nitric oxide functions as a potent antioxidant againstmethylviologen-mediated damage to lipids,proteins and RNAM.V. Beligni, L. LamattinaInstituto de Investigaciones Biolo´gicas (IIB), Facultad deCiencias Exactas y Naturales, Universidad Nacional de Mardel Plata, CC 1245, 7600 Mar del Plata, Argentina.Fax: (54) 223 475 3150; E-mail: lolama@mdp.edu.arOxidative stress within chloroplasts is commonly generated dueto an imbalance in light-dependent O2 reduction. This is exacerbatedby methylviologen herbicides, such as diquat, that act atphotosystem I as artificial electron acceptors. Reactive oxygen speciesthat are overproduced provoke severe damage to the plant cell.Here we report that two nitric oxide (NO) donors, sodium nitroprusside(SNP) and S-nitroso-N-acetylpenicillamine (SNAP), greatly reducedlipid peroxidation and protein loss caused by the applicationof a high dose of diquat to potato leaves or isolated chloroplasts. SNPprotective effect was abolished when it was added together withcarboxy-PTIO, an NO scavenger. Nitric oxide protection againstprotein loss was extremely noticeable for rubisco large subunit(LSU) and D1 protein of photosystem II. Diquat also caused massiveRNA breakdown by 10 h after application to the leaves. Moreover,the amount of LSU mRNA, but not that of D1, was reduced bydiquat even before the whole RNA population was affected. Nitricoxide donors also reverted LSU mRNA decrease and protectedagainst general RNA breakdown until 13 h after diquat treatment.Diquat-mediated increase in the rate of chloroplastic electron transportwas also restored to control values by NO. These resultsstrengthen our previous reports on the ability of NO to act asantioxidant in plants and add new evidence of its functionality in theplant kingdom.