Toxicity Evaluation of copper oxide nanoparticles
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Toxicity Evaluation of Copper Oxide Nanoparticles
Introduction to Copper Oxide Nanoparticles (CuO NPs) Toxicity
Copper oxide nanoparticles (CuO NPs) are widely used in various applications, including antimicrobial agents, electronics, and catalysis. However, their increasing use raises concerns about their potential toxicity to both human health and the environment. This article synthesizes recent research findings on the toxicity mechanisms of CuO NPs across different biological systems.
Oxidative Stress and Apoptosis in Mammalian Cells
Hepatotoxicity in Rats and Hepatocytes
Studies have shown that CuO NPs induce significant oxidative stress and endoplasmic reticulum (ER) stress, leading to hepatotoxicity and apoptosis in mammalian cells. In male Wistar rats, intranasal instillation of CuO NPs resulted in liver function impairment, oxidative stress, inflammatory responses, and histopathological damage1. Similarly, in vitro experiments on rat hepatocytes (BRL-3A cells) demonstrated that CuO NP exposure led to excessive reactive oxygen species (ROS) production, decreased mitochondrial membrane potential, and apoptosis1.
Cytotoxicity in Human Hepatoma Cells
In human hepatoma (HepG2) cells, CuO NPs were found to cause increased cytotoxicity, mutagenicity, oxidative stress, and mitochondrial impairment. The production of ROS and superoxide anions was significantly higher with prolonged exposure, indicating that the liver is a primary target for CuO NP toxicity7.
Mechanisms of Toxicity in Aquatic Organisms
Effects on Blue Mussels
CuO NPs have been shown to induce dose-dependent toxic effects in the blue mussel, Mytilus edulis. The nanoparticles caused protein oxidation, histological changes, and oxidative stress in gill tissues, comparable to the effects of other toxic metal oxide nanoparticles like chromium and cobalt3.
Impact on Aquatic Plants
In the aquatic plant Myriophyllum spicatum, CuO NPs were less toxic than Cu salts, despite similar internal Cu concentrations. The difference in toxicity was attributed to the progressive leaching of Cu2+ ions from CuO NPs, representing a chronic exposure, as opposed to the acute exposure from Cu salts4.
Toxicity in Artemia salina
CuO NPs exhibited significant toxicity in different life stages of Artemia salina, with the median lethal concentration (LC50) values varying across developmental stages. The primary cause of toxicity was the accumulation of Cu nanoparticles in the gut, leading to biochemical changes and oxidative stress5.
Cellular and Molecular Mechanisms
Role of Surface Modifications
The cytotoxicity of CuO NPs can be influenced by surface modifications. For instance, CuO NPs with different surface coatings (e.g., sodium citrate, polyvinylpyrrolidone) showed varying levels of cytotoxicity in murine macrophage cells. The toxicity was not directly linked to particle dissolution or ROS production but rather to the synergistic interactions between the nanoparticles and their coatings6.
Protein Oxidation and Cellular Uptake
In the blue mussel, CuO NPs caused protein oxidation and cellular uptake, leading to oxidative stress and histological changes. The presence of CuO NPs in gill tissues was confirmed through proteomic analysis, which identified several oxidized proteins3.
Environmental and Ecological Implications
Toxicity in Freshwater Organisms
CuO NPs pose significant ecological risks to freshwater organisms. For example, the Neotropical species Ceriodaphnia silvestrii and Hyphessobrycon eques showed decreased reproduction, feeding inhibition, and increased ROS generation when exposed to CuO NPs. The toxicity was primarily induced by the nanoparticles rather than the released copper ions9.
Phytotoxicity in Soybean Plants
In soil-grown soybean plants, CuO NPs caused particle size- and concentration-dependent toxicity, affecting seed yield and antioxidant defense systems. Smaller nanoparticles (25 nm) were more toxic than larger ones (50 nm and 250 nm), indicating a size-dependent toxicity mechanism10.
Conclusion
Copper oxide nanoparticles exhibit significant toxicity across various biological systems, primarily through mechanisms involving oxidative stress, protein oxidation, and cellular uptake. The toxicity is influenced by factors such as particle size, surface modifications, and exposure duration. Understanding these mechanisms is crucial for developing safer nanomaterials and mitigating their environmental and health impacts.
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Most relevant research papers on this topic
Exposure to copper oxide nanoparticles triggers oxidative stress and endoplasmic reticulum (ER)-stress induced toxicology and apoptosis in male rat liver and BRL-3A cell.
Copper oxide nanoparticles cause liver damage and apoptosis by triggering oxidative stress and endoplasmic reticulum stress, leading to cell death in liver tissue and BRL-3A cells.
Non-RCT
Animal Study
Highly CitedCytotoxic origin of copper(II) oxide nanoparticles: comparative studies with micron-sized particles, leachate, and metal salts.
Copper oxide nanoparticles' cytotoxicity comes from complexation-mediated leaching by amino acids, highlighting the importance of materials toxicity at the nanoscale.
In Vitro StudyHighly CitedToxicity of copper oxide nanoparticles in the blue mussel, Mytilus edulis: a redox proteomic investigation.
Copper oxide nanoparticles induce dose-dependent toxic effects in the blue mussel, Mytilus edulis, with similar toxicity to toxic metal oxide nanoparticles like chromium and cobalt.
Non-RCTAnimal StudyHighly CitedCutting-edge spectroscopy techniques highlight toxicity mechanisms of copper oxide nanoparticles in the aquatic plant Myriophyllum spicatum.
Copper oxide nanoparticles are less toxic to aquatic plants than copper salt, with the difference in toxicity coming from sudden massive Cu2+ addition from Cu salt versus progressive leaching from CuO-NPs.
Non-RCTToxicity and accumulation of Copper oxide (CuO) nanoparticles in different life stages of Artemia salina.
Copper oxide nanoparticles are toxic to Artemia salina, with accumulation in the gut being the major cause of toxicity.
Toxicity of surface-modified copper oxide nanoparticles in a mouse macrophage cell line: Interplay of particles, surface coating and particle dissolution.
Surface-modified copper oxide nanoparticles show varying cytotoxicity, with PEI-coated NPs being the most cytotoxic, but their dissolution and coating agent toxicity play a synergistic role in their toxicity.
In Vitro StudyCytotoxicity, mutagenicity, oxidative stress and mitochondrial impairment in human hepatoma (HepG2) cells exposed to copper oxide, copper-iron oxide and carbon nanoparticles.
Copper oxide nanoparticles are highly toxic to human HepG2 cells, suggesting the liver as a target organ for their toxicity.
In Vitro StudyEvaluation of toxicity and oxidative stress induced by copper oxide nanoparticles in the green alga Chlamydomonas reinhardtii.
Copper oxide nanoparticles (CuO NP) can cause growth inhibition, decreased carotenoids levels, and oxidative stress in Chlamydomonas reinhardtii, causing toxic responses from 0.1 mg L(-1) after 72 hours of treatment.
In Vitro StudyHighly CitedToxicity of copper oxide nanoparticles to Neotropical species Ceriodaphnia silvestrii and Hyphessobrycon eques.
Copper oxide nanoparticles cause toxic effects on Neotropical species Ceriodaphnia silvestrii and Hyphessobrycon eques, with reactive oxidative species playing a key role in the toxicity pathway.
In Vitro StudyParticle size and concentration dependent toxicity of copper oxide nanoparticles (CuONPs) on seed yield and antioxidant defense system in soil grown soybean (Glycinemax cv. Kowsar).
Copper oxide nanoparticles (CuONPs) show differential nano-specific toxicity compared to ionic Cu2+ toxicity in soybean, with CuONP-25 showing higher inhibition of antioxidant biomarkers than larger size CuONPs or Cu2+ ions.
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