Abstract

Concentration of engineered nickel oxide nanoparticle (NiO-NP) in nature is on the rise, owing to large scale industrial uses, which have accreted the scope of its exposure to plants, the primary producers of the ecosystem. Though an essential micronutrient for the animal system, supported by numerous studies confirming its toxicity at higher dosages, nickel oxide is graded as a human carcinogen by WHO. A few studies do depict toxicity and bioaccumulation of nickel in plants; however, interaction of NiO-NP with plants is not well-elucidated. It is known that exposure to NiO-NP can incite stress response, leading to cytotoxicity and growth retardation in some plants, but a defined work on the intricate physicochemical cellular responses and genotoxic challenges is wanting. The present study was planned to explore cytotoxicity of NiO-NP in the model plant, Allium cepa L., its internalization in the tissue and concomitant furore created in the antioxidant enzyme system of the plant. The prospect of the NiO-NP causing genotoxicity was also investigated. Detailed assessments biochemical profiles and genotoxicity potential of NiO-NP on A. cepa L. was performed and extended to four of its closest economically important relatives, Allium sativum L., Allium schoenoprasum L., Allium porrum L., and Allium fistulosum L. Growing root tips were treated with seven different concentrations of NiO-NP suspension (10–500 mg L−1), with deionised distilled water as negative control and 0.4 mM EMS solution as positive control. Study of genotoxic endpoints, like, mitotic indices (MI), chromosomal aberrations (CAs), and chromosome breaks confirmed NiO-NP induced genotoxicity in plants, even at a very low dose (10 mg L−1). That NiO-NP also perturbs biochemical homeostasis, disrupting normal physiology of the cell, was confirmed through changes in state of lipid peroxidation malonaldehyde (MDA), as well as, in oxidation marker enzymes, like catalase (CAT), super oxide dismutase (SOD), and guiacol peroxidase (POD) activities. It was evident that increase in NiO-NP concentration led to decrease in MIs in all the study materials, concomitant with a spike of stress-alleviating, antioxidant enzymes-CAT, POD, SOD, and significant increase in MDA formation. Hence, it can be confirmed that NiO-NP should be treated as an environmental hazard.

Highlights

  • Widespread use of engineered nanoparticles (ENPs) in consumer products has given way to their release and accumulation in the environment, where they are readily taken up by living systems inciting stress (Burklew et al, 2012; Maurer-Jones et al, 2013; Tripathi et al, 2016a)

  • Transmission Electron Microscopy (TEM) analysis was performed to elucidate and evaluate size, as well as, distribution of nickel oxide nanoparticle (NiO-NP), while Dynamic Light Scattering (DLS) analysis helped study the physical parameters in aqueous suspension

  • Aqueous suspension of NiO-NP studied through DLS showed high rate of agglomeration, as indicated from distribution curves in water (Figure 1C)

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Summary

Introduction

Widespread use of engineered nanoparticles (ENPs) in consumer products has given way to their release and accumulation in the environment, where they are readily taken up by living systems inciting stress (Burklew et al, 2012; Maurer-Jones et al, 2013; Tripathi et al, 2016a) Due to their small sizes (100 nm in at least one dimension) and large surface-area to volume ratio, ENPs have close association with living organisms in their surrounding environment; plants, primary component of any ecosystem, have the most dynamic interactions with them. Though plant interaction with ENPs predominantly results in phytotoxicity, especially at high concentrations, e.g., in tomato, cabbage, carrot, pea, and lettuce, some reports do indicate that exposure to ENPs promoted growth in onion and cucumber (Cañas et al, 2008; Stampoulis et al, 2009; Tripathi et al, 2017c). DNA damage is presumed to be induced either due to direct intercalation of ENPs or their physical and/or electrochemical interaction with DNA, as well as, ROS-mediated damage (Atha et al, 2012)

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