Toxicological Assessment of Quantum Dot Nanoparticles

Quantum dot nanoparticles are semiconductor nanocrystals whose size-tunable optical and electronic properties have accelerated their use in biomedical imaging, diagnostics and emerging therapeutic applications. These materials typically comprise a core of cadmium-based or indium-based semiconductor encased within a shell and surface ligands that govern colloidal stability and biological interactions. Toxicological assessment addresses a broad range of in vitro and in vivo end points, including cytotoxicity, oxidative stress, inflammation, immunotoxicity, genotoxicity and organ biodistribution. Key determinants of hazard include particle size, composition, surface charge, coating chemistry and dose. Oxidative stress driven by reactive oxygen species and heavy metal ion release can provoke apoptosis, ferroptosis and organelle dysfunction such as mitophagy. In vivo studies reveal accumulation in liver, spleen and lung with slow clearance and potential for long-term retention. Recent efforts focus on developing cadmium-free formulations, optimising surface ligands for minimal platelet activation and enhancing biocompatibility. A robust framework for characterising physicochemical properties alongside standardised biological assays is essential to ensure safe translation and global regulatory acceptance.

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Toxicological Assessment of Quantum Dot Nanoparticles publication trend

The graph below shows the total number of articles in toxicological assessment of quantum dot nanoparticles across all publications each year (not limited to Nature Index journals).

Technical terms

Quantum dot (QD): nanoscale semiconductor crystal that emits size-dependent light upon excitation, used in imaging and sensing.

Surface ligand: organic molecule bound to the nanoparticle shell that modulates solubility, stability and interaction with biomolecules.

Biocompatibility: ability of a material to perform with an appropriate host response without eliciting adverse effects.

Reactive oxygen species (ROS): highly reactive molecules containing oxygen that can damage lipids, proteins and DNA.

Ferroptosis: regulated cell death driven by iron-dependent lipid peroxidation and glutathione depletion.

Mitophagy: selective autophagic removal of damaged mitochondria to maintain cellular health.

References

1. Quantum Dots‐caused Retinal Degeneration in Zebrafish Regulated by Ferroptosis and Mitophagy in Retinal Pigment Epithelial Cells through Inhibiting Spliceosome. Advanced Science (2024).
2. Impact of Surface Ligand on the Biocompatibility of InP/ZnS Quantum Dots with Platelets. Small (2023).
3. Exploring the potential and safety of quantum dots in allergy diagnostics. Microsystems & Nanoengineering (2023).
4. A Toxicologic Review of Quantum Dots: Toxicity Depends on Physicochemical and Environmental Factors. Environmental Health Perspectives (2005).