Nitric oxide protects carbon assimilation process of watermelon from boron-induced oxidative injury

Nitric oxide protects carbon assimilation process of watermelon from boron-induced oxidative injury
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一氧化氮保护西瓜的碳同化过程免受硼诱导的氧化损伤

DOI:
10.1016/j.plaphy.2016.11.024
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发表时间:
2017-02-01
影响因子:
6.5
通讯作者:
Fang, Zhang Ming
Fang, Zhang Ming
中科院分区:
生物学2区
文献类型:
--
作者:
Farag, Mohamed;Najeeb, Ullah;Fang, Zhang Ming

文献摘要

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Nitric oxide (NO) mediates plant response to a variety of abiotic stresses; however, limited information is available on its effect on boron (B)-stressed watermelon plants. The present study investigates the mechanism through which NO protects watermelon seedlings from B deficiency and toxicity stresses. Five days old watermelon seedlings were exposed to B (0, 0.5 and 10 mg L-1) alone or with 75 mole of NO donor sodium nitroprusside (SNP) for 30 days. Both low and high B concentrations in the media altered nutrient accumulation and impaired various physiological processes of watermelon seedlings, leading to a significant reduction in biomass production. The plants exposed to B deficient or toxic concentrations had 66 and 69% lower shoot dry weight, respectively compared with optimum B levels. B toxicity-induced growth inhibition of watermelon seedlings was associated with high B translocation to shoot tissues, which caused lipid membrane peroxidation (12% increase) and chlorophyll destruction (25% reduction). In contrast, B deficiency accelerated generation of reactive oxygen species (ROS), specifically OH-1 and induced cellular oxidative injury. Exogenously applied SNP promoted leaf chlorophyll, photosynthesis and consequently biomass production in B-stressed watermelon seedlings by reducing B accumulation, lipid membrane peroxidation and ROS generation. It also activated antioxidant enzymes such as SOD, POD and APX, and protected the seedlings from ROS-induced cellular burst. (C) 2016 Published by Elsevier Masson SAS.