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

被引:161
作者
Beligni, MV [1 ]
Lamattina, L [1 ]
机构
[1] Univ Mar del Plata, Fac Ciencias Exactas & Nat, Inst Invest Biol, RA-7600 Mar Del Plata, Argentina
来源
NITRIC OXIDE-BIOLOGY AND CHEMISTRY | 1999年 / 3卷 / 03期
关键词
nitric oxide; methylviologen herbicides; reactive oxygen species; chlorophyll loss; cell death; Solanum tuberosum;
D O I
10.1006/niox.1999.0222
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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 Boss. 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 mu M 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. (C) 1999 Academic Press.
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页码:199 / 208
页数:10
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