Liver Toxicity of Cadmium Telluride Quantum Dots (CdTe QDs) Due to Oxidative Stress in Vitro and in Vivo.

Ting Zhang,Jiali Ying,Yuanyuan Hu,Meng Tang,Yuepu Pu,Lu Kong,Yuying Xue,Tianshu Wu

doi:10.3390/ijms161023279

Ting Zhang, Jiali Ying + Show 6 more

Open Access

https://doi.org/10.3390/ijms161023279

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Abstract

With the applications of quantum dots (QDs) expanding, many studies have described the potential adverse effects of QDs, yet little attention has been paid to potential toxicity of QDs in the liver. The aim of this study was to investigate the effects of cadmium telluride (CdTe) QDs in mice and murine hepatoma cells alpha mouse liver 12 (AML 12). CdTe QDs administration significantly increased the level of lipid peroxides marker malondialdehyde (MDA) in the livers of treated mice. Furthermore, CdTe QDs caused cytotoxicity in AML 12 cells in a dose- and time-dependent manner, which was likely mediated through the generation of reactive oxygen species (ROS) and the induction of apoptosis. An increase in ROS generation with a concomitant increase in the gene expression of the tumor suppressor gene p53, the pro-apoptotic gene Bcl-2 and a decrease in the anti-apoptosis gene Bax, suggested that a mitochondria mediated pathway was involved in CdTe QDs’ induced apoptosis. Finally, we showed that NF-E2-related factor 2 (Nrf2) deficiency blocked induced oxidative stress to protect cells from injury induced by CdTe QDs. These findings provide insights into the regulatory mechanisms involved in the activation of Nrf2 signaling that confers protection against CdTe QDs-induced apoptosis in hepatocytes.

Highlights

With the development of nanotechnology, numerous nanomaterials have been created for a variety of applications
The oxidative stress in the livers of mice and alpha mouse liver 12 (AML 12) cells exposed to cadmium telluride (CdTe) quantum dots (QDs) was measured, and the potential mechanisms of toxicity were evaluated
After treatment with CdTe QDs, AML 12 cells showed an increase in Reactive Oxygen Species (ROS) generation and apoptosis, with a concomitant increase in the gene expression of tumor suppressor gene p53 and pro-apoptotic gene Bcl-2, as well as a decrease in the anti-apoptosis gene expression Bax, suggesting that a mitochondria-mediated pathway is involved in CdTe QD-induced apoptosis

Summary

Introduction

With the development of nanotechnology, numerous nanomaterials have been created for a variety of applications. Quantum dots (QDs) are one of the most promising developments among these nanomaterials, because their unique autofluorescence properties have great potential in biomedicine for diagnosis, drug delivery, and imaging [1]. QDs have great potential in terms of clinical applications, they have been shown to cause adverse effects in vitro and in vivo and have potential risks for human health. QDs can be distributed to all body systems and can be aggregated in some tissues and organs [2,3,4]. The assessment of the health risk of QDs to the human body is based upon the level of exposure, the toxicity of the material in question, the route of exposure and the persistence of the particular material in the organism. A number of studies have investigated the biodistribution of QDs and their whole body clearance after intravenous administration, and found that the liver is to be a major accumulation site for circulatory

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