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

Durgesh Kumar Tripathi, Rohit Kumar Mishra, Swati Singh, Samiksha Singh, Kanchan Vishwakarma, Shivesh Sharma, Vijay Pratap Singh, Prashant Kumar Singh, Sheo Mohan Prasad, Nawal Kishore Dubey,

Frontiers in Plant Science · 2017 · 1.2K citations · 45 references

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TL;DR

The study examines whether nitric oxide mitigates zinc oxide nanoparticle toxicity in wheat seedlings. Zinc oxide nanoparticles reduced wheat seedling growth, photosynthetic efficiency, and AsA‑GSH antioxidant activity while increasing Zn accumulation, H₂O₂, and lipid peroxidation; nitric oxide supplied via SNP partially restored photosynthesis, lowered Zn accumulation, preserved antioxidant enzyme activities, and its protective effect was abrogated by an NO scavenger.

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.

References

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