Abstract
The dynamic interplay between toxicity pathways (oxidative stress, calcium disturbances, genetic damage) caused by nanoparticles and the repair mechanisms of inhibition of cell division and induction of cell death is explored in zebrafish embryo cells.
Highlights
Silver nanoparticles (AgNPs) are one of the most commonly used nanomaterials in consumer products, primarily due to their antimicrobial properties that have been widely exploited in a diverse range of consumer products, such as soaps, pastes, textiles, and other health sector goods.[1]
Environmental Science: Nano often results in increased intracellular reactive oxygen species (ROS), which can be generated in multiple organelles, as a result of an imbalance between ROS production and their scavenging and a decrease in the phase II antioxidant defence enzymes, such as superoxide dismutase (SOD), catalase (CAT), and glutathione reductase (GR).[2,3]
As part of our efforts to elucidate the interactions of AgNPs with fish cellular models, we evaluated the potential use of commercial embryonic zebrafish cells (ZF4) as an emerging in vitro toxicological model
Summary
Silver nanoparticles (AgNPs) are one of the most commonly used nanomaterials in consumer products, primarily due to their antimicrobial properties that have been widely exploited in a diverse range of consumer products, such as soaps, pastes, textiles, and other health sector goods.[1]. The physicochemical characteristics (e.g., size, surface area and charge) of nanoparticles (NPs) influence their internalisation by cells and determine their cytotoxicity as the internalized NPs interact with organelles, potentially disrupting the cellular equilibrium and triggering stress-related responses.[2] This redox imbalance within cells Paper. Environmental Science: Nano often results in increased intracellular reactive oxygen species (ROS), which can be generated in multiple organelles, as a result of an imbalance between ROS production and their scavenging and a decrease in the phase II antioxidant defence enzymes, such as superoxide dismutase (SOD), catalase (CAT), and glutathione reductase (GR).[2,3] Intracellular ROS can act as messengers or mediators in many cellular signalling processes, having an essential role in cell life and death decisions. ROS overload and the associated disruption of biological process may induce disruption of deoxyribonucleic acid (DNA), proteins, lipids, and other macromolecules.[7]
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