PUBLICATION
Acute and sub-lethal exposure to copper oxide nanoparticles causes oxidative stress and teratogenicity in zebrafish embryos
- Authors
- Ganesan, S., Anaimalai Thirumurthi, N., Raghunath, A., Vijayakumar, S., Perumal, E.
- ID
- ZDB-PUB-151024-8
- Date
- 2016
- Source
- Journal of applied toxicology : JAT 36(4): 554-67 (Journal)
- Registered Authors
- Azhwar, Raghunath
- Keywords
- CuO-NPs, oxidative stress, sub-lethal exposure, teratogenicity, zebrafish embryos
- MeSH Terms
-
- Acetylcholinesterase/metabolism
- Animals
- Antioxidants/pharmacology
- Apoptosis
- Copper/chemistry
- Copper/toxicity*
- Embryo, Nonmammalian/drug effects
- Embryo, Nonmammalian/metabolism
- Heart Rate/drug effects
- Nanoparticles/chemistry
- Nanoparticles/toxicity*
- Oxidative Stress/drug effects*
- Reactive Oxygen Species/metabolism
- Sodium-Potassium-Exchanging ATPase/metabolism
- Teratogenesis/drug effects*
- Toxicity Tests, Acute
- Toxicity Tests, Chronic
- Zebrafish/embryology*
- PubMed
- 26493272 Full text @ J. Appl. Toxicol.
- CTD
- 26493272
Citation
Ganesan, S., Anaimalai Thirumurthi, N., Raghunath, A., Vijayakumar, S., Perumal, E. (2016) Acute and sub-lethal exposure to copper oxide nanoparticles causes oxidative stress and teratogenicity in zebrafish embryos. Journal of applied toxicology : JAT. 36(4):554-67.
Abstract
Nano-copper oxides are a versatile inorganic material. As a result of their versatility, the immense applications and usage end up in the environment causing a concern for the lifespan of various beings. The ambiguities surround globally on the toxic effects of copper oxide nanoparticles (CuO-NPs). Hence, the present study endeavored to study the sub-lethal acute exposure effects on the developing zebrafish embryos. The 48 hpf LC50 value was about 64 ppm. Therefore, we have chosen the sub-lethal dose of 40 and 60 ppm for the study. Accumulation of CuO-NPs was evidenced from the SEM-EDS and AAS analyzes. The alterations in the AChE and Na(+) /K(+) -ATPase activities disrupted the development process. An increment in the levels of oxidants with a concomitant decrease in the antioxidant enzymes confirmed the induction of oxidative stress. Oxidative stress triggered apoptosis in the exposed embryos. Developmental anomalies were observed with CuO-NPs exposure in addition to oxidative stress in the developing embryos. Decreased heart rate and hatching delay hindered the normal developmental processes. Our work has offered valuable data on the connection between oxidative stress and teratogenicity leading to lethality caused by CuO-NPs. A further molecular mechanism unraveling the uncharted connection between oxidative stress and teratogenicity will aid in the safe use of CuO-NPs.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping