Abstract
Nanotechnology has emerged as a powerful field of applied research. However, the potential toxicity of nano-materials is a cause of concern. A thorough toxicological investigation is required before a nanomaterial is evaluated for application of any kind. In this context, there is concerted effort to find appropriate test systems to assess the toxicity of nanomaterials. Toxicity of a nanomaterial greatly depends on its physicochemical properties and the biological system with which it interacts. The present research was carried out with a view to generate data on eco-toxicological impacts of copper oxide nanorod (CuO NR) in Hydra magnipapillata 105 at organismal, cellular and molecular levels. Exposure of hydra to CuO NR resulted in severe morphological alterations in a concentration- as well as duration-dependent manner. Impairment of feeding, population growth, and regeneration was also observed. In vivo and in vitro analyses revealed induction of oxidative stress, genotoxicity, and molecular machinery of apoptotic cell death, accompanied by disruption of cell cycle progression. Taken together, CuO nanorod is potentially toxic to the biological systems. Also, hydra offers potential to be used as a convenient model organism for aquatic ecotoxicological risk assessment of nanomaterials.
Highlights
The toxicity pathways without relying on the laboratory animal models[13]
The synthesized CuO nanorod (CuO NR) was dispersed in water and the suspension was scanned with the wavelength range of 200 to 900 nm in an UV-Vis Spectrophotometer, which showed a broad absorption peak at 296 nm (Fig. 1A)
At the lower concentration the transcripts levels of genes CAT, Glucose-6-phosphate dehydrogenase (G6PD), Glutathione S-transferase (GST), and SOD exhibited overlapping expression and the increased expression of the GPx and Glutathione reductase (GR) genes, observed at 12 h, decreased to normal level at 24 and 48 h which suggest that these genes do not play any significant role when the exposure is to a concentration lesser than the threshold. These findings suggest that exposure of hydra to a higher concentration of CuO NR increased the susceptibility to cell death by way of increased ROS generation and failure of the antioxidant defense system, whereas following exposure to a lower concentration of CuO NR hydra produced counteracting antioxidant defense system to neutralize the enhanced oxidative stress and activated the adaptive mechanisms by up-regulating the stress-responsive gene Hsp[70]
Summary
The toxicity pathways without relying on the laboratory animal models[13]. The common conclusion drawn from various in vitro studies testified that CuO nanoparticles induce cytotoxicity through DNA damage and oxidative stress leading to apoptotic cell death[14,15,16]. Ecotoxicological risk assessment of CuO nanomaterials mainly focuses on aquatic organisms[10]. From the aquatic habitats they can access the terrestrial animals and the humans through food chain and inflict toxicity[19]. Several studies have been conducted on aquatic organisms such as daphnia, zebrafish and artemia for assessing the toxicity of CuO nanoparticles[21,22,23], the toxicity of CuO nanorod (NR) has not yet been evaluated. For the present study we chose Hydra magnipapillata 105, a simple freshwater organism belonging to phylum Cnidaria, as the model to evaluate the detrimental effects of CuO NR. All the cells in hydra are in contact with the aqueous environment which facilitates permeation of toxic substances into the animal[29,30]. The entire genome of hydra having been sequenced, the recent advances in molecular biological techniques enabled us to decipher the mechanisms underlying CuO NR toxicity in hydra from morphopysiological, cellular and molecular perspectives
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