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 damage. 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 apoptosis.
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 toxicity.
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 cobalt.
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 salts.
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 stress.
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 coatings.
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 proteins.
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 ions.
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 mechanism.
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.
Cytotoxic origin of copper(II) oxide nanoparticles: comparative studies with micron-sized particles, leachate, and metal salts.
Toxicity of copper oxide nanoparticles in the blue mussel, Mytilus edulis: a redox proteomic investigation.
Cutting-edge spectroscopy techniques highlight toxicity mechanisms of copper oxide nanoparticles in the aquatic plant Myriophyllum spicatum.
Toxicity and accumulation of Copper oxide (CuO) nanoparticles in different life stages of Artemia salina.
Toxicity of surface-modified copper oxide nanoparticles in a mouse macrophage cell line: Interplay of particles, surface coating and particle dissolution.
Cytotoxicity, mutagenicity, oxidative stress and mitochondrial impairment in human hepatoma (HepG2) cells exposed to copper oxide, copper-iron oxide and carbon nanoparticles.
Evaluation of toxicity and oxidative stress induced by copper oxide nanoparticles in the green alga Chlamydomonas reinhardtii.
Toxicity of copper oxide nanoparticles to Neotropical species Ceriodaphnia silvestrii and Hyphessobrycon eques.
Particle size and concentration dependent toxicity of copper oxide nanoparticles (CuONPs) on seed yield and antioxidant defense system in soil grown soybean (Glycinemax cv. Kowsar).
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