Cytotoxicity of gold nanoclusters in human liver&amp;nbsp;cancer cells

Yang, Yanjie; Jing, Nan; Hou, Jianwen; Yu, Bianfei; Zhao, Tong; Xu, Shengwen; Lv, Shuangyu; Zhang, Haixia

doi:10.2147/ijn.s69013

Cited by 15 publications

(11 citation statements)

References 28 publications

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“…This uptake did not translate into significant cytotoxicity after 24 h of exposure. The latter is consistent with 3.2 nm dihydrolipoic-coated gold nanoclusters (24.5 µg/mL) causing no toxicity in the normal human liver L02 cell line after 72 h of exposure 62,63. In contrast, production of pro-inflammatory cytokines has been demonstrated in primary rat hepatocytes after 4 h of incubation with 20 nm AuNPs (211.2 µg/mL), showing a higher sensitivity than liver macrophages 64.…”

Section: Discussionsupporting

confidence: 79%

<p>Gold nanoparticles affect the antioxidant status in selected normal human cells</p>

Daems¹,

Penninckx²,

Nelissen³

et al. 2019

IJN

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Purpose: This study evaluates the cytotoxicity of AuNPs coated with polyallylamine (AuNPs-PAA) and conjugated or not to the epidermal growth factor receptor (EGFR)-targeting antibody Cetuximab (AuNPs-PAA-Ctxb) in normal human kidney (HK-2), liver (THLE-2) and microvascular endothelial (TIME) cells, and compares it with two cancer cell lines that are EGFR-overexpressing (A431) or EGFR-negative (MDA-MB-453). Results: Conjugation of Cetuximab to AuNPs-PAA increased the AuNPs-PAA-Ctxb interactions with cells, but reduced their cytotoxicity. TIME cells exhibited the strongest reduction in viability after exposure to AuNPs-PAA(±Ctxb), followed by THLE-2, MDA-MB-453, HK-2 and A431 cells. This cell type-dependent sensitivity was strongly correlated to the inhibition of thioredoxin reductase (TrxR) and glutathione reductase (GR), and to the depolarization of the mitochondrial membrane potential. Both are suggested to initiate apoptosis, which was indeed detected in a concentration- and time-dependent manner. The role of oxidative stress in AuNPs-PAA(±Ctxb)-induced cytotoxicity was demonstrated by co-incubation of the cells with N-acetyl L-cysteine (NAC), which significantly decreased apoptosis and mitochondrial membrane depolarization. Conclusion: This study helps to identify the cells and tissues that could be sensitive to AuNPs and deepens the understanding of the risks associated with the use of AuNPs in vivo.

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Section: Discussionsupporting

confidence: 79%

<p>Gold nanoparticles affect the antioxidant status in selected normal human cells</p>

Daems¹,

Penninckx²,

Nelissen³

et al. 2019

IJN

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“…The viability assay showed that the growth inhibitory rates of nanosilver to HepG2 cells were time- and dose-dependent, while L02 cell viability was not affected at a concentration of nanosilver below 80 µg mL −1 for 24 h. The result indicated that HepG2 cells are more sensitive than are L02 cells when exposed to nanosilver under the same concentration. Others 39 had similar results with HepG2 and L02 cells treated with gold nanoclusters. The toxicity of nanosilver reportedly depends largely on the release of silver ions.…”

Section: Discussionmentioning

confidence: 59%

Comparative cytotoxicity and apoptotic pathways induced by nanosilver in human liver HepG2 and L02 cells

et al. 2018

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Silver nanoparticles are used in many commercial products in daily life. Exposure to nanosilver has hepatotoxic effects in animals. This study investigated the cytotoxicity associated with polyvinylpyrrolidone-coated nanosilver (23.44 ± 4.92 nm in diameter) exposure in the human hepatoma cell line (HepG2) and normal hepatic cell line (L02), and the molecular mechanisms induced by nanosilver in HepG2 cells. Nanosilver, in doses of 20-160 μg mL for 24 and 48 h, reduced cell viability in a dose- and time-dependent manner and induced cell membrane leakage and mitochondria injury in both cell lines; these effects were more pronounced in HepG2 cells than in L02 cells. Intracellular oxidative stress was documented by reactive oxygen species (ROS) being generated in HepG2 cells but not in L02 cells, an effect possibly due to differential uptake of nanosilver by cancer cells and normal cells. In HepG2 cells, apoptosis was documented by finding that ROS triggered a decrease in mitochondrial membrane potential, an increase in cytochrome c release, activation of caspase 3 and caspase 9, and a decrease in the ratio of Bcl-2/Bax. Furthermore, nanosilver activated the Fas death receptor pathway by downregulation of nuclear factor-κB and activation of caspase 8 and caspase 3. These results suggest that apoptosis induced by nanosilver in HepG2 cells is mediated via a mitochondria-dependent pathway and the Fas death receptor pathway. These findings provide toxicological and mechanistic information that can help in assessing the effects of nanosilver in biological systems, including the potential for anticancer activities.

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“…To evaluate the potential application of the constructed MIP nanoparticles in DDS, the cytotoxicity tests of MIP and N-MIL on HepG2 cells and HL-7702 cells [ 41 , 42 , 43 , 44 , 45 , 46 ] were detected by MTT method ( Figure 8 ). The cell viability showed that the inhibition rate increased with time increasing.…”

Section: Resultsmentioning

confidence: 99%

Molecularly Imprinting Polymers (MIP) Based on Nitrogen Doped Carbon Dots and MIL-101(Fe) for Doxorubicin Hydrochloride Delivery

et al. 2020

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MIL-based molecularly imprinted polymer (MIP) nanocomposites were successfully synthesized through a simple and versatile stirring auxiliary encapsulation method. MIP as a carrier has been applied to the highly efficient selective recognition and sustained release of doxorubicin hydrochloride (DOX). The adsorption mechanism and release behavior of MIP@DOX in vitro were also discussed. Adsorption studies showed that MIP using DOX as template had specific selectivity to DOX, and its optimal drug loading efficiency reached 97.99%. The adsorption isotherm accorded with Freundlich models. The cumulative release curve showed that at the conditions of pH 5.5 and 7.4, the nanomaterials have a slow-release effect on the release of DOX. In addition, the cytotoxicity and bioactivity of MIP nanoparticles on HepG2 and HL-7702 cell lines measured by MTT assay also proved their low toxicity and biological activity. The cell activity of HepG2 and HL-7702 incubated with MIP for 24 h was 69.9% and 76.07%, respectively. These results collectively illustrated that the MIP nano-materials synthesized in this study can be efficiently employed to the drug delivery systems.

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Cytotoxicity of gold nanoclusters in human liver cancer cells

Cited by 15 publications

References 28 publications

<p>Gold nanoparticles affect the antioxidant status in selected normal human cells</p>

<p>Gold nanoparticles affect the antioxidant status in selected normal human cells</p>

Comparative cytotoxicity and apoptotic pathways induced by nanosilver in human liver HepG2 and L02 cells

Molecularly Imprinting Polymers (MIP) Based on Nitrogen Doped Carbon Dots and MIL-101(Fe) for Doxorubicin Hydrochloride Delivery

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