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Front Plant Sci. 2017 Feb 6;8:1. doi: 10.3389/fpls.2017.00001. eCollection 2017.

Nitric Oxide Ameliorates Zinc Oxide Nanoparticles Phytotoxicity in Wheat Seedlings: Implication of the Ascorbate-Glutathione Cycle.

Author information

1
Centre of Advanced in Botany, Banaras Hindu University VaranasiVaranasi, India; Centre for Medical Diagnostic and Research, Motilal Nehru National Institute of TechnologyAllahabad, India.
2
Centre for Medical Diagnostic and Research, Motilal Nehru National Institute of Technology Allahabad, India.
3
D D Pant Interdisciplinary Research Lab, Department of Botany, University of Allahabad Allahabad, India.
4
Ranjan Plant Physiology and Biochemistry Laboratory, Department of Botany, University of Allahabad Allahabad, India.
5
Department of Biotechnology, Motilal Nehru National Institute of Technology Allahabad, India.
6
Centre for Medical Diagnostic and Research, Motilal Nehru National Institute of TechnologyAllahabad, India; Department of Biotechnology, Motilal Nehru National Institute of TechnologyAllahabad, India.
7
Government Ramanuj Pratap Singhdev Post Graduate College Koriya, India.
8
Nanotechnology Application Centre, University of Allahabad Allahabad, India.
9
Centre of Advanced in Botany, Banaras Hindu University Varanasi Varanasi, India.
10
Department of Biology, Western Kentucky University, Bowling Green KY, USA.

Abstract

The present study investigates ameliorative effects of nitric oxide (NO) against zinc oxide nanoparticles (ZnONPs) phytotoxicity in wheat seedlings. ZnONPs exposure hampered growth of wheat seedlings, which coincided with reduced photosynthetic efficiency (Fv/Fm and qP), due to increased accumulation of zinc (Zn) in xylem and phloem saps. However, SNP supplementation partially mitigated the ZnONPs-mediated toxicity through the modulation of photosynthetic activity and Zn accumulation in xylem and phloem saps. Further, the results reveal that ZnONPs treatments enhanced levels of hydrogen peroxide and lipid peroxidation (as malondialdehyde; MDA) due to severely inhibited activities of the following ascorbate-glutatione cycle (AsA-GSH) enzymes: ascorbate peroxidase, glutathione reductase, monodehydroascorbate reductase and dehydroascorbate reductase, and its associated metabolites ascorbate and glutathione. In contrast to this, the addition of SNP together with ZnONPs maintained the cellular functioning of the AsA-GSH cycle properly, hence lesser damage was noticed in comparison to ZnONPs treatments alone. The protective effect of SNP against ZnONPs toxicity on fresh weight (growth) can be reversed by 2-(4carboxy-2-phenyl)-4,4,5,5-tetramethyl- imidazoline-1-oxyl-3-oxide, a NO scavenger, and thus suggesting that NO released from SNP ameliorates ZnONPs toxicity. Overall, the results of the present study have shown the role of NO in the reducing of ZnONPs toxicity through the regulation of accumulation of Zn as well as the functioning of the AsA-GSH cycle.

KEYWORDS:

DNA damage; ZnONPs; amelioration; ascorbate–glutathione cycle; nanotoxicity; nitric oxide

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