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ZnO Nanoparticles Treatment Induces Apoptosis by Increasing Intracellular ROS Levels in LTEP-a-2 Cells.

Wang C, Hu X, Gao Y, Ji Y - Biomed Res Int (2015)

Bottom Line: Both intracellular reactive oxygen species (ROS) and reduced glutathione (GSH) were examined by a microplate-reader method.Results showed that ZnO NPs (≥ 0.01 μg/mL) significantly inhibited proliferation (P < 0.05) and induced substantial apoptosis in LTEP-a-2 cells after 4 h of exposure.The intracellular ROS level rose up to 30-40% corresponding to significant depletion (approximately 70-80%) in GSH content in LTEP-a-2 cells (P < 0.05), suggesting that ZnO NPs induced apoptosis mainly through increased ROS production.

View Article: PubMed Central - PubMed

Affiliation: Key Laboratory of Coastal Biology and Bioresource Utilization, Yantai Institute of Coastal Zone Research, Chinese Academy of Sciences, 17 Chunhui Road, Laishan District, Yantai 264003, China ; University of Chinese Academy of Sciences, Beijing 100049, China.

ABSTRACT
Owing to the wide use of novel nanoparticles (NPs) such as zinc oxide (ZnO) in all aspects of life, toxicological research on ZnO NPs is receiving increasing attention in these days. In this study, the toxicity of ZnO NPs in a human pulmonary adenocarcinoma cell line LTEP-a-2 was tested in vitro. Log-phase cells were exposed to different levels of ZnO NPs for hours, followed by colorimetric cell viability assay using tetrazolium salt and cell survival rate assay using trypan blue dye. Cell morphological changes were observed by Giemsa staining and light microscopy. Apoptosis was detected by using fluorescence microscopy and caspase-3 activity assay. Both intracellular reactive oxygen species (ROS) and reduced glutathione (GSH) were examined by a microplate-reader method. Results showed that ZnO NPs (≥ 0.01 μg/mL) significantly inhibited proliferation (P < 0.05) and induced substantial apoptosis in LTEP-a-2 cells after 4 h of exposure. The intracellular ROS level rose up to 30-40% corresponding to significant depletion (approximately 70-80%) in GSH content in LTEP-a-2 cells (P < 0.05), suggesting that ZnO NPs induced apoptosis mainly through increased ROS production. This study elucidates the toxicological mechanism of ZnO NPs in human pulmonary adenocarcinoma cells and provides reference data for application of nanomaterials in the environment.

No MeSH data available.


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Depletion of intracellular glutathione (GSH) in LTEP-a-2 cells after 4 h of exposure to ZnO nanoparticles (0 μg/mL, control). GSH content determined by spectrophotometry. *P < 0.05, **P < 0.01 versus control by Student's t-test.
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fig7: Depletion of intracellular glutathione (GSH) in LTEP-a-2 cells after 4 h of exposure to ZnO nanoparticles (0 μg/mL, control). GSH content determined by spectrophotometry. *P < 0.05, **P < 0.01 versus control by Student's t-test.

Mentions: GSH is one of the most abundant intracellular antioxidant thiols, which is involved in cell redox homeostasis and is central to defensive mechanisms against toxic agents and oxidant-mediated injury [36, 37]. In the present study, the GSH content significantly declined in LTEP-a-2 cells exposed to ZnO NPs (0.01–0.25 μg/mL) for 4 h compared with the control cells (P < 0.05, Figure 7). The depletion of GSH coincided with the enlarging tendency of intracellular ROS level (Figure 6) once again demonstrating that ZnO NPs damaged the antioxidant mechanism of LTEP-a-2 cells.


ZnO Nanoparticles Treatment Induces Apoptosis by Increasing Intracellular ROS Levels in LTEP-a-2 Cells.

Wang C, Hu X, Gao Y, Ji Y - Biomed Res Int (2015)

Depletion of intracellular glutathione (GSH) in LTEP-a-2 cells after 4 h of exposure to ZnO nanoparticles (0 μg/mL, control). GSH content determined by spectrophotometry. *P < 0.05, **P < 0.01 versus control by Student's t-test.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4538331&req=5

fig7: Depletion of intracellular glutathione (GSH) in LTEP-a-2 cells after 4 h of exposure to ZnO nanoparticles (0 μg/mL, control). GSH content determined by spectrophotometry. *P < 0.05, **P < 0.01 versus control by Student's t-test.
Mentions: GSH is one of the most abundant intracellular antioxidant thiols, which is involved in cell redox homeostasis and is central to defensive mechanisms against toxic agents and oxidant-mediated injury [36, 37]. In the present study, the GSH content significantly declined in LTEP-a-2 cells exposed to ZnO NPs (0.01–0.25 μg/mL) for 4 h compared with the control cells (P < 0.05, Figure 7). The depletion of GSH coincided with the enlarging tendency of intracellular ROS level (Figure 6) once again demonstrating that ZnO NPs damaged the antioxidant mechanism of LTEP-a-2 cells.

Bottom Line: Both intracellular reactive oxygen species (ROS) and reduced glutathione (GSH) were examined by a microplate-reader method.Results showed that ZnO NPs (≥ 0.01 μg/mL) significantly inhibited proliferation (P < 0.05) and induced substantial apoptosis in LTEP-a-2 cells after 4 h of exposure.The intracellular ROS level rose up to 30-40% corresponding to significant depletion (approximately 70-80%) in GSH content in LTEP-a-2 cells (P < 0.05), suggesting that ZnO NPs induced apoptosis mainly through increased ROS production.

View Article: PubMed Central - PubMed

Affiliation: Key Laboratory of Coastal Biology and Bioresource Utilization, Yantai Institute of Coastal Zone Research, Chinese Academy of Sciences, 17 Chunhui Road, Laishan District, Yantai 264003, China ; University of Chinese Academy of Sciences, Beijing 100049, China.

ABSTRACT
Owing to the wide use of novel nanoparticles (NPs) such as zinc oxide (ZnO) in all aspects of life, toxicological research on ZnO NPs is receiving increasing attention in these days. In this study, the toxicity of ZnO NPs in a human pulmonary adenocarcinoma cell line LTEP-a-2 was tested in vitro. Log-phase cells were exposed to different levels of ZnO NPs for hours, followed by colorimetric cell viability assay using tetrazolium salt and cell survival rate assay using trypan blue dye. Cell morphological changes were observed by Giemsa staining and light microscopy. Apoptosis was detected by using fluorescence microscopy and caspase-3 activity assay. Both intracellular reactive oxygen species (ROS) and reduced glutathione (GSH) were examined by a microplate-reader method. Results showed that ZnO NPs (≥ 0.01 μg/mL) significantly inhibited proliferation (P < 0.05) and induced substantial apoptosis in LTEP-a-2 cells after 4 h of exposure. The intracellular ROS level rose up to 30-40% corresponding to significant depletion (approximately 70-80%) in GSH content in LTEP-a-2 cells (P < 0.05), suggesting that ZnO NPs induced apoptosis mainly through increased ROS production. This study elucidates the toxicological mechanism of ZnO NPs in human pulmonary adenocarcinoma cells and provides reference data for application of nanomaterials in the environment.

No MeSH data available.


Related in: MedlinePlus