Necrotic cell death induced by the protein-mediated intercellular uptake of CdTe quantum dots

Lai, Lu; Jin, Jian-Cheng; Xu, Ziqiang; Mei, Ping; Jiang, Feng-Lei; Liu, Yi

doi:10.1016/j.chemosphere.2015.04.044

Cited by 48 publications

(25 citation statements)

References 43 publications

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“…The interaction between CdTe QDs and PRV also lead to the release of Cd 2+ , which was detected by Inductively Coupled Plasma Optical Emission Spectrometry (ICP-OES) 42 . The results indicated that 4.1 ± 0.3 μM Cd 2+ was released when PRV was exposed to 80 nM GSH-CdTe QDs (624 nm).…”

Section: Resultsmentioning

confidence: 99%

Probing the interactions of CdTe quantum dots with pseudorabies virus

Cai

Han

et al. 2015

Sci Rep

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Quantum dots (QDs) have become one of the most promising luminescent materials for tracking viral infection in living cells. However, several issues regarding how QDs interact with the virus remain unresolved. Herein, the effects of Glutathione (GSH) capped CdTe QDs on virus were investigated by using pseudorabies virus (PRV) as a model. One-step growth curve and fluorescence colocalization analyses indicate that CdTe QDs inhibit PRV multiplication in the early stage of virus replication cycle by suppressing the invasion, but have no significant effect on the PRV penetration. Fluorescence spectrum analysis indicates that the size of QDs is reduced gradually after the addition of PRV within 30 min. Release of Cd2+ was detected during the interaction of QDs and PRV, resulting in a decreased number of viruses which can infect cells. Further Raman spectra and Circular Dichroism (CD) spectroscopy analyses reveal that the structure of viral surface proteins is altered by CdTe QDs adsorbed on the virus surface, leading to the inhibition of virus replication. This study facilitates an in-depth understanding of the pathogenic mechanism of viruses and provides a basis for QDs-labeled virus research.

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Section: Resultsmentioning

confidence: 99%

Probing the interactions of CdTe quantum dots with pseudorabies virus

Cai

Han

et al. 2015

Sci Rep

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“…After that, QDs translocate in cells via endocytic vesicles and then are rapidly degraded in lysosomes, leading to cell necrosis. Therefore, considering the cytotoxicity mechanism of CdTe QDs can provide valuable data for the safe use of QDs in the future [108].…”

Section: Pathways Of Np-triggered Necrosismentioning

confidence: 99%

Necrotic, apoptotic and autophagic cell fates triggered by nanoparticles

et al. 2018

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Nanomaterials have gained a rapid increase in use in a variety of applications that pertain to many aspects of human life. The majority of these innovations are centered on medical applications and a range of industrial and environmental uses ranging from electronics to environmental remediation. Despite the advantages of NPs, the knowledge of their toxicological behavior and their interactions with the cellular machinery that determines cell fate is extremely limited. This review is an attempt to summarize and increase our understanding of the mechanistic basis of nanomaterial interactions with the cellular machinery that governs cell fate and activity. We review the mechanisms of NP-induced necrosis, apoptosis and autophagy and potential implications of these pathways in nanomaterial-induced outcomes. Abbreviations: Ag, silver; CdTe, cadmium telluride; CNTs, carbon nanotubes; EC, endothelial cell; GFP, green fluorescent protein; GO, graphene oxide; GSH, glutathione; HUVECs, human umbilical vein endothelial cells; NP, nanoparticle; PEI, polyethylenimine; PVP, polyvinylpyrrolidone; QD, quantum dot; ROS, reactive oxygen species; SiO, silicon dioxide; SPIONs, superparamagnetic iron oxide nanoparticles; SWCNT, single-walled carbon nanotubes; TiO, titanium dioxide; USPION, ultra-small super paramagnetic iron oxide; ZnO, zinc oxide.

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“…Several reports about ultrafine particulate matter-induced necrotic cell death have been published. 32 Necrosis induced by QDs 33,34 has also been found, while necroptosis has not been reported.…”

Section: Necrosismentioning

confidence: 99%

Dysfunction of various organelles provokes multiple cell death after quantum dot exposure

Wang

Tang

2018

IJN

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Quantum dots (QDs) are different from the materials with the micrometer scale. Owing to the superiority in fluorescence and optical stability, QDs act as possible diagnostic and therapeutic tools for application in biomedical field. However, potential threats of QDs to human health hamper their wide utilization in life sciences. It has been reported that oxidative stress and inflammation are involved in toxicity caused by QDs. Recently, accumulating research unveiled that disturbance of subcellular structures plays a magnificent role in cytotoxicity of QDs. Diverse organelles would collapse during QD treatment, including DNA damage, endoplasmic reticulum stress, mitochondrial dysfunction and lysosomal rupture. Different forms of cellular end points on the basis of recent research have been concluded. Apart from apoptosis and autophagy, a new form of cell death termed pyroptosis, which is finely orchestrated by inflammasome complex and gasdermin family with secretion of interleukin-1 beta and interleukin-18, was also summarized. Finally, several potential cellular signaling pathways were also listed. Activation of Toll-like receptor-4/myeloid differentiation primary response 88, nuclear factor kappa-light-chain-enhancer of activated B cells and NACHT, LRR and PYD domains-containing protein 3 inflammasome pathways by QD exposure is associated with regulation of cellular processes. With the development of QDs, toxicity evaluation is far behind its development, where specific mechanisms of toxic effects are not clearly defined. Further studies concerned with this promising area are urgently required.

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Necrotic cell death induced by the protein-mediated intercellular uptake of CdTe quantum dots

Cited by 48 publications

References 43 publications

Probing the interactions of CdTe quantum dots with pseudorabies virus

Probing the interactions of CdTe quantum dots with pseudorabies virus

Necrotic, apoptotic and autophagic cell fates triggered by nanoparticles

Dysfunction of various organelles provokes multiple cell death after quantum dot exposure

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