Quantum dots induce heat shock-related cytotoxicity at intracellular environment

Migita, Satoshi; Moquin, Alexandre; Fujishiro, Hitomi; Himeno, Seiichiro; Maysinger, Dušica; Winnik, Françoise M.; Taniguchi, Akiyoshi

doi:10.1007/s11626-013-9693-2

Cited by 10 publications

(7 citation statements)

References 35 publications

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“…Excessive production of ROS was one of the common mechanisms for the toxic effects of nanomaterials; the ROS can react with macromolecules such as proteins, DNA, lipids etc., which affects the structure and function of macromolecules, and then causes cell oxidative damage (Cho et al, ; Juzenas, Generalov, Juzeniene, & Moan, ; Kermanizadeh, Gaiser, Johnston, Brown, & Stone, ; L. Liu et al, ; Migita et al, ; Skalickova et al, ; Tsay & Michalet, ; Wang & Tang, ; Wang, Gao, & Su, ; Yong & Swihart, ). The Tang et al study outcomes showed that CdTe QDs and cadmium chloride caused ROS to increase significantly in zebrafish liver cells, which lead to DNA strand breaks, meanwhile, antioxidant genes and DNA repair gene expression was significantly upregulated (Tang, Allagadda, et al, ).…”

Section: Toxic Effects Of Quantum Dotsmentioning

confidence: 99%

“…Excessive production of ROS was one of the common mechanisms for the toxic effects of nanomaterials; the ROS can react with macromolecules such as proteins, DNA, lipids etc., which affects the structure and function of macromolecules, and then causes cell oxidative damage (Cho et al, 2007;Juzenas, Generalov, Juzeniene, & Moan, 2008;Kermanizadeh, Gaiser, Johnston, Brown, & Stone, 2014;L. Liu et al, 2015;Migita et al, 2014;Skalickova et al, 2013;Tsay & Michalet, 2005;Wang & Tang, 2018;Wang, Gao, & Su, 2010;Yong & Swihart, 2012 Bcl-2 were obviously downregulated, ATG3, ATG7, ATG13 and ATG14 were upregulated, AIFM2, APAF1 and BAD were upregulated. Paesano et al, 2016 Realgar QDs: 5.48 nm HepG2 cells 0-80 μg ml −1 Cell death and MMP decreased in a dose-dependent manner, IC 50 for HepG2 after 6 h was 23 μg ml −1 ;Bcl-2 showed dose-dependent decrease and Bax was increased at the level of gene and protein;ER stress gene GRP78 and CHOP increased by 30-and 10-fold, respectively.…”

Section: Reactive Oxygen Species and Oxidative Stressmentioning

confidence: 99%

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Review of toxicological effect of quantum dots on the liver

Tang

Zhang

2018

J of Applied Toxicology

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In recent years, quantum dots (QDs) have potential applications in technology, research and medicine. The small particle size is coupled to their unique chemical and physical properties and their excellent fluorescence characteristics. A growing number of studies have shown that QDs are distributed to secondary organs through multiple pathways, while the liver is the main reservoir of QDs. Here, we review current liver toxicity studies of QDs in vivo and in vitro. Mechanisms of hepatotoxicity are discussed and the problem of extrapolating knowledge gained from cell-based studies into animal studies is highlighted. In this context, there still exists significant discrepancies between in vitro and in vivo results, and the specific toxicity mechanism remains unclear. The hepatotoxicities of QDs are the need for a unifying protocol for reliable and realistic toxicity reports.

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Section: Toxic Effects Of Quantum Dotsmentioning

confidence: 99%

“…Excessive production of ROS was one of the common mechanisms for the toxic effects of nanomaterials; the ROS can react with macromolecules such as proteins, DNA, lipids etc., which affects the structure and function of macromolecules, and then causes cell oxidative damage (Cho et al, 2007;Juzenas, Generalov, Juzeniene, & Moan, 2008;Kermanizadeh, Gaiser, Johnston, Brown, & Stone, 2014;L. Liu et al, 2015;Migita et al, 2014;Skalickova et al, 2013;Tsay & Michalet, 2005;Wang & Tang, 2018;Wang, Gao, & Su, 2010;Yong & Swihart, 2012 Bcl-2 were obviously downregulated, ATG3, ATG7, ATG13 and ATG14 were upregulated, AIFM2, APAF1 and BAD were upregulated. Paesano et al, 2016 Realgar QDs: 5.48 nm HepG2 cells 0-80 μg ml −1 Cell death and MMP decreased in a dose-dependent manner, IC 50 for HepG2 after 6 h was 23 μg ml −1 ;Bcl-2 showed dose-dependent decrease and Bax was increased at the level of gene and protein;ER stress gene GRP78 and CHOP increased by 30-and 10-fold, respectively.…”

Section: Reactive Oxygen Species and Oxidative Stressmentioning

confidence: 99%

Review of toxicological effect of quantum dots on the liver

Tang

Zhang

2018

J of Applied Toxicology

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“…1 Several transcriptomic analyses indicate that exposure to any stress agents, especially to toxic compounds, prompts changes in gene expression profile, especially genes related to stress response 2-4 , reactive oxygen species (ROS) metabolic processes 2 , 3 , DNA damage response 2 , and cell redox homeostasis 2 . In order to maintain cellular integrity and survival, nanomaterial exposure (i.e., silver nanoparticles (NPs) 5 , silica NPs 6 , quantum dots (QDs) 7 , or carbon nanotubes 8 ) triggers the production of a set of heat shock proteins (HSPs). 9 The HSPs are a sub-group of molecular chaperons; accessory proteins that manage mechanisms crucial for the cell survival and maintenance including protein folding and assembly mechanisms.…”

Section: Introductionmentioning

confidence: 99%

Genetic Circuits to Detect Nanomaterial Triggered Toxicity through Engineered Heat Shock Response Mechanism

Saltepe

Hacıosmanoğlu

Şeker

2018

Preprint

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Biocompatibility assessment of nanomaterials has been of great interest due to their potential toxicity. However, conventional biocompatibility tests are short of providing a fast toxicity report. We developed a whole cell based biosensor to track biocompatibility of nanomaterials with the aim of providing fast feedback for engineering nanomaterials with lower toxicity levels. We have engineered promoters of four heat shock response proteins. As an initial design a reporter coding gene was cloned to downstream of the promoter regions selected. Initial results indicated that native HSP promoter regions were not very promising to generate signals with low background signals. Introducing riboregulators to native promoters eliminated unwanted background signal almost entirely. Unfortunately, this approach also leads a decrease in expected sensor signal. Thus, a repression based genetic circuit, inspired 2 from HSP mechanism of Mycobacterium tuberculosis was constructed. These genetic circuits can report the toxicity of Quantum Dot nanoparticles in one hour with high precision. Our designed nanoparticle toxicity sensors can provide quick reports which can lower the demand for additional experiments with more complex organisms. gene. 10,14 Under steady state conditions, sigma 32 level is maintained at constant levels due to its unstable nature; however, after exposure to any stress, sigma 32 level is dramatically elevated via improved stability as well as increased synthesis. 10,15,16 Sigma 32 is regulated by a negative feedback loop controlled by DnaK-DnaJ-GrpE mechanism. 17 Accumulation of chaperones in this mechanism holds sigma 32 and blocks its activity 18,19 , leading to degradation of sigma 32 by FtsH; a special sigma 32 degrading protease. 20 Therefore, monitoring of HSP levels in cells can be used as a promising stress indicator.Nanomaterials are of great interest for their wide range of applicability across many areas from medicine to optoelectronics. Nanoparticles have size-dependent tunable optical and physical properties; which are not usual for bulk materials 21-23 , nanomaterials are widely used in innovative applications such as in medical diagnostics, drug delivery and targeted photothermal therapy. In all of these approaches patients have to be exposed to nanomaterials. 24 Also, utilization of nanomaterials in consumer goods may contaminate environment, food and textiles. 25 Despite their success in many applications, nanomaterials' high surface-tovolume ratio indicates potential health problems. In addition, due to their small size, nanomaterials are able to penetrate through cellular barriers easily which may cause cellular stress and many adverse effects such as protein unfolding 26 , DNA damage 27,28 , ROS generation 29-31 , and disruption of gene expression 27,28,32 . At the system level, nanomaterials can trigger inflammation and alter immune system response [33][34][35] . Thus, development of a quick and reliable sensor system that reports nanomaterial-triggered toxicity is very critica...

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“…In order to maintain cellular integrity and survival, nanomaterial exposure ( i.e. , silver nanoparticles (NPs), silica NPs, quantum dots (QDs), or carbon nanotubes) triggers the production of a set of HSPs . The HSPs are a subgroup of molecular chaperones: accessory proteins that manage mechanisms crucial for the cell survival and maintenance including protein folding and assembly mechanisms .…”

mentioning

confidence: 99%

Genetic Circuits To Detect Nanomaterial Triggered Toxicity through Engineered Heat Shock Response Mechanism

et al. 2019

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Biocompatibility assessment of nanomaterials has been of great interest due to their potential toxicity. However, conventional biocompatibility tests fall short of providing a fast toxicity report. We developed a whole cell based biosensor to track biocompatibility of nanomaterials with the aim of providing fast feedback to engineer them with lower toxicity levels. We engineered promoters of four heat shock response (HSR) proteins utilizing synthetic biology approaches. As an initial design, a reporter coding gene was cloned downstream of the selected promoter regions. Initial results indicated that native heat shock protein (HSP) promoter regions were not very promising to generate signals with low background signals. Introducing riboregulators to native promoters eliminated unwanted background signals almost entirely. Yet, this approach also led to a decrease in expected sensor signal upon stress treatment. Thus, a repression based genetic circuit, inspired by the HSR mechanism of Mycobacterium tuberculosis, was constructed. These genetic circuits could report the toxicity of quantum dot nanoparticles in 1 h. Our designed nanoparticle toxicity sensors can provide quick reports, which can lower the demand for additional experiments with more complex organisms.

show abstract

Quantum dots induce heat shock-related cytotoxicity at intracellular environment

Cited by 10 publications

References 35 publications

Review of toxicological effect of quantum dots on the liver

Review of toxicological effect of quantum dots on the liver

Genetic Circuits to Detect Nanomaterial Triggered Toxicity through Engineered Heat Shock Response Mechanism

Genetic Circuits To Detect Nanomaterial Triggered Toxicity through Engineered Heat Shock Response Mechanism

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