The protective effects of resveratrol, H 2 S and thermotherapy on the cell apoptosis induced by CdTe quantum dots

Wu, Tianshu; Zhan, Qingling; Zhang, Ting; Ang, Shengjun; Ying, Jiali; He, Keyu; Zhang, Shihan; Yang, Xue; Tang, Meng

doi:10.1016/j.tiv.2017.02.013

Cited by 14 publications

(4 citation statements)

References 58 publications

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“…In our opinion, the concentrations of Cd may be a better index for determining the toxicity of QDs than the molar concentration of the QD particles. The differences among the molar concentrations of the three QDs were large, but according to our former study, there was a narrow difference in cytotoxicity between the 2.2 and 3.5 nm QDs (Wu et al, ; Wu, He, Zhan, Ang, et al, ; Wu, et al, ). Therefore, we recommend the use of Cd concentrations as an indicator among laboratories worldwide.…”

Section: Discussionmentioning

confidence: 79%

DNA damage in BV‐2 cells: An important supplement to the neurotoxicity of CdTe quantum dots

Wei

et al. 2018

J of Applied Toxicology

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Microglial cells are resident immune cells in the central nervous system. Activation of microglia as induced by CdTe quantum dots (QDs) can trigger damage to neurons. To quantify the intracellular QDs, we monitored the intracellular Cd concentration in the QD‐exposed mouse microglial cells (BV‐2 cell line). The extent of cell injury at different times correlated with the Cd concentration in cells at that time. In addition to Cd ion detection, we also monitored the intracellular fluorescence of the QDs. More QDs accumulated in the nucleus than in the cytoplasm. Comet assays confirmed that QDs induce DNA damage. However, DNA cannot interact with QDs, so the DNA damage was not caused by CdTe QDs adducts to DNA but by the increase of the Cd ion concentration and the secondary oxidative damage. In addition to DNA damage, biofilm injury and endogenous reduced glutathione depletion were also apparent in QD‐exposed BV‐2 cells. These changes can be prevented or even reversed by exogenous reduced glutathione administration.

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Section: Discussionmentioning

confidence: 79%

DNA damage in BV‐2 cells: An important supplement to the neurotoxicity of CdTe quantum dots

Wei

et al. 2018

J of Applied Toxicology

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“…Previous studies have confirmed that nanoparticles, especially QDs, are ideal materials for early neural tracing, and the application of QDs has particularly attracted widespread attention (Chen & Liang, 2020). Although QDs have many advantages and benefits for neural tracing, it is still essential to ensure their biological safety of the nervous system before applying QDs (Wu et al, 2017). Unfortunately, there are few studies on the peripheral neurotoxicology of QDs, which makes it valuable for us to study the neurotoxicity of CdTe QDs in peripheral nerve cells.…”

Section: Discussionmentioning

confidence: 99%

The apoptosis induced by CdTe quantum dots through the mitochondrial pathway in dorsal root ganglion cell line ND7/23

Bai

Wei

Zou

et al. 2022

J of Applied Toxicology

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Recently, the use of CdTe quantum dots in the field of biomedicine, such as biological imaging, biosensors, cell markers, and drug carriers, is increasing due to their special physical and chemical properties. However, their biosafety assessment lags far behind their rapid application. In this study, we observed that CdTe quantum dots with certain exposed doses and time decreased the cell viability and increased the apoptosis rates in ND7/23 cells. In general, CdTe quantum dots exposure could promote the accumulation of reactive oxygen species (ROS) in cells and decrease the mitochondrial membrane potential, which led to pathological changes and subcellular organelle damages. We hypothesized that the mitochondrial pathway could be involved in CdTe quantum dots-induced apoptosis. The results suggested that CdTe quantum dots exposure increased the expression levels of three mitochondrial pathway markers, for example, caspase-3, cytochrome c, and Bax while decreased Bcl-2

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“…Studies have identified oxidative stress as one of the toxicity mechanisms of QDs and cadmium-based QDs have been shown to cause excessive accumulation of ROS, indirectly triggering adverse outcomes. 302–305 CdTe QDs can trigger mitochondrial dysfunction in hepatocytes via ROS, leading to apoptosis, 306 and CdSe/ZnS QDs can lead to ROS accumulation, altered phagocytosis, and increased apoptosis in macrophages. 211 The excessive accumulation of ROS generated by QDs which can mediate not only the induction of apoptosis but also other forms of ROS-mediated cell death can also be triggered, such as autophagy, 307–312 inflammation, 201,203,216,313–316 pyroptosis, 203,214,316 necrosis, 317–319 and ferroptosis.…”

Section: Toxicity Mechanism Of Qdsmentioning

confidence: 99%

New insights into the safety assessment of quantum dots: potential release pathways, environmental transformations, and health risks

Liu

Ding

Pang

et al. 2022

Environ. Sci.: Nano

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The protective effects of resveratrol, H 2 S and thermotherapy on the cell apoptosis induced by CdTe quantum dots

Cited by 14 publications

References 58 publications

DNA damage in BV‐2 cells: An important supplement to the neurotoxicity of CdTe quantum dots

DNA damage in BV‐2 cells: An important supplement to the neurotoxicity of CdTe quantum dots

The apoptosis induced by CdTe quantum dots through the mitochondrial pathway in dorsal root ganglion cell line ND7/23

New insights into the safety assessment of quantum dots: potential release pathways, environmental transformations, and health risks

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