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Ecotoxicology and Environmental Safety 2016-Nov

Salicylic acid mediates antioxidant defense system and ABA pathway related gene expression in Oryza sativa against quinclorac toxicity.

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Jian Wang
Mengting Lv
Faisal Islam
Rafaqat A Gill
Chong Yang
Basharat Ali
Guijun Yan
Weijun Zhou

Anahtar kelimeler

Öz

The auxin herbicide quinclorac is widely used for controlling weeds in transplanted and direct-seeded rice fields. However, its phytotoxic responses on rice are still unknown. Therefore, in the present investigation we studied the effects of different concentrations (0, 0.1 and 0.5g/L) of quinclorac herbicide on the physiological and biochemical changes of two rice cultivars (XS 134 and ZJ 88) and further analyzed the ameliorating role of salicylic acid (SA) on quinclorac toxicity in rice plants. The results revealed that exogenous application of SA significantly increased plant biomass and total chlorophyll contents in herbicide stressed plants. The lipid peroxidation and ROS (H2O2, O2(-.), (-)OH) production were significantly increased in roots and leaves of both rice cultivars under quinclorac stress, demonstrating an oxidative burst in rice plants. Whereas, application of SA significantly lowered ROS contents under quinclorac stress. Further, exogenous SA treatment significantly modulated antioxidant enzymes and enhanced GSH concentration in stress plants. Anatomical observations of leaf and root revealed that herbicide affected internal structures, while SA played a vital role in protection from toxic effects. Expression analysis of stress hormone ABA genes (OsABA8oxs, OsNCEDs) revealed that quinclorac application enhanced stress condition in cultivar ZJ 88, while SA treatment downregulated ABA genes more in cultivar XS 134, which correlated with the enhanced tolerance to quinclorac induced oxidative stress in this cultivar. The present study delineated that SA played a critical role under quinclorac stress in both rice cultivars by regulating antioxidant defense system, reducing ROS formation and preventing the degradation of internal cell organelles.

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