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Zinc oxide nanoparticles induce oxidative DNA damage and ROS-triggered mitochondria mediated apoptosis in human liver cells (HepG2)

The wide scale use of Zinc oxide (ZnO) nanoparticles in the world consumer market makes human beings more prone to the exposure to ZnO nanoparticles and its adverse effects. The liver, which is the primary organ of metabolism, might act as a major target organ for ZnO nanoparticles after they gain e... Full description

Journal Title: Apoptosis (London) 2012, Vol.17 (8), p.852-870
Main Author: Sharma, Vyom
Other Authors: Anderson, Diana , Dhawan, Alok
Format: Electronic Article Electronic Article
Language: English
Subjects:
DNA
Publisher: Boston: Springer US
ID: ISSN: 1360-8185
Link: https://www.ncbi.nlm.nih.gov/pubmed/22395444
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title: Zinc oxide nanoparticles induce oxidative DNA damage and ROS-triggered mitochondria mediated apoptosis in human liver cells (HepG2)
format: Article
creator:
  • Sharma, Vyom
  • Anderson, Diana
  • Dhawan, Alok
subjects:
  • Antioxidants - pharmacology
  • Apoptosis
  • Apoptosis - drug effects
  • Apoptosis Regulatory Proteins - metabolism
  • Biochemistry
  • Biomedical and Life Sciences
  • Biomedicine
  • Cancer Research
  • Cell Biology
  • Cell death
  • Cell Survival - drug effects
  • Cells
  • DNA
  • DNA Damage
  • Enzyme Inhibitors - pharmacology
  • general
  • Hep G2 Cells
  • Humans
  • L-Lactate Dehydrogenase - metabolism
  • Lipid Peroxidation
  • Membrane Potential, Mitochondrial
  • Mitochondria, Liver - drug effects
  • Mitochondria, Liver - metabolism
  • Mitochondrial DNA
  • Mitogen-Activated Protein Kinases - antagonists & inhibitors
  • Mitogen-Activated Protein Kinases - metabolism
  • Mutagens - toxicity
  • Nanoparticles
  • Nanoparticles - toxicity
  • Nanoparticles - ultrastructure
  • Nanotechnology
  • Oncology
  • Original Paper
  • Oxidation-Reduction
  • Oxidative Stress
  • Particle Size
  • Phosphorylation
  • Physiological aspects
  • Protein Processing, Post-Translational
  • Reactive Oxygen Species - metabolism
  • Tumor proteins
  • Virology
  • Zinc oxide
  • Zinc Oxide - metabolism
  • Zinc Oxide - pharmacology
  • Zinc Oxide - toxicity
ispartof: Apoptosis (London), 2012, Vol.17 (8), p.852-870
description: The wide scale use of Zinc oxide (ZnO) nanoparticles in the world consumer market makes human beings more prone to the exposure to ZnO nanoparticles and its adverse effects. The liver, which is the primary organ of metabolism, might act as a major target organ for ZnO nanoparticles after they gain entry into the body through any of the possible routes. Therefore, the aim of the present study was to assess the apoptotic and genotoxic potential of ZnO nanoparticles in human liver cells (HepG2) and the underlying molecular mechanism of its cellular toxicity. The role of dissolution in the toxicity of ZnO nanoparticles was also investigated. Our results demonstrate that HepG2 cells exposed to 14–20 μg/ml ZnO nanoparticles for 12 h showed a decrease in cell viability and the mode of cell death induced by ZnO nanoparticles was apoptosis. They also induced DNA damage which was mediated by oxidative stress as evidenced by an increase in Fpg sensitive sites. Reactive oxygen species triggered a decrease in mitochondria membrane potential and an increase in the ratio of Bax/Bcl2 leading to mitochondria mediated pathway involved in apoptosis. In addition, ZnO nanoparticles activated JNK, p38 and induced p53 Ser15 phosphorylation. However, apoptosis was found to be independent of JNK and p38 pathways. This study investigating the effects of ZnO nanoparticles in human liver cells has provided valuable insights into the mechanism of toxicity induced by ZnO nanoparticles.
language: eng
source:
identifier: ISSN: 1360-8185
fulltext: no_fulltext
issn:
  • 1360-8185
  • 1573-675X
url: Link


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titleZinc oxide nanoparticles induce oxidative DNA damage and ROS-triggered mitochondria mediated apoptosis in human liver cells (HepG2)
creatorSharma, Vyom ; Anderson, Diana ; Dhawan, Alok
creatorcontribSharma, Vyom ; Anderson, Diana ; Dhawan, Alok
descriptionThe wide scale use of Zinc oxide (ZnO) nanoparticles in the world consumer market makes human beings more prone to the exposure to ZnO nanoparticles and its adverse effects. The liver, which is the primary organ of metabolism, might act as a major target organ for ZnO nanoparticles after they gain entry into the body through any of the possible routes. Therefore, the aim of the present study was to assess the apoptotic and genotoxic potential of ZnO nanoparticles in human liver cells (HepG2) and the underlying molecular mechanism of its cellular toxicity. The role of dissolution in the toxicity of ZnO nanoparticles was also investigated. Our results demonstrate that HepG2 cells exposed to 14–20 μg/ml ZnO nanoparticles for 12 h showed a decrease in cell viability and the mode of cell death induced by ZnO nanoparticles was apoptosis. They also induced DNA damage which was mediated by oxidative stress as evidenced by an increase in Fpg sensitive sites. Reactive oxygen species triggered a decrease in mitochondria membrane potential and an increase in the ratio of Bax/Bcl2 leading to mitochondria mediated pathway involved in apoptosis. In addition, ZnO nanoparticles activated JNK, p38 and induced p53 Ser15 phosphorylation. However, apoptosis was found to be independent of JNK and p38 pathways. This study investigating the effects of ZnO nanoparticles in human liver cells has provided valuable insights into the mechanism of toxicity induced by ZnO nanoparticles.
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languageeng
publisherBoston: Springer US
subjectAntioxidants - pharmacology ; Apoptosis ; Apoptosis - drug effects ; Apoptosis Regulatory Proteins - metabolism ; Biochemistry ; Biomedical and Life Sciences ; Biomedicine ; Cancer Research ; Cell Biology ; Cell death ; Cell Survival - drug effects ; Cells ; DNA ; DNA Damage ; Enzyme Inhibitors - pharmacology ; general ; Hep G2 Cells ; Humans ; L-Lactate Dehydrogenase - metabolism ; Lipid Peroxidation ; Membrane Potential, Mitochondrial ; Mitochondria, Liver - drug effects ; Mitochondria, Liver - metabolism ; Mitochondrial DNA ; Mitogen-Activated Protein Kinases - antagonists & inhibitors ; Mitogen-Activated Protein Kinases - metabolism ; Mutagens - toxicity ; Nanoparticles ; Nanoparticles - toxicity ; Nanoparticles - ultrastructure ; Nanotechnology ; Oncology ; Original Paper ; Oxidation-Reduction ; Oxidative Stress ; Particle Size ; Phosphorylation ; Physiological aspects ; Protein Processing, Post-Translational ; Reactive Oxygen Species - metabolism ; Tumor proteins ; Virology ; Zinc oxide ; Zinc Oxide - metabolism ; Zinc Oxide - pharmacology ; Zinc Oxide - toxicity
ispartofApoptosis (London), 2012, Vol.17 (8), p.852-870
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descriptionThe wide scale use of Zinc oxide (ZnO) nanoparticles in the world consumer market makes human beings more prone to the exposure to ZnO nanoparticles and its adverse effects. The liver, which is the primary organ of metabolism, might act as a major target organ for ZnO nanoparticles after they gain entry into the body through any of the possible routes. Therefore, the aim of the present study was to assess the apoptotic and genotoxic potential of ZnO nanoparticles in human liver cells (HepG2) and the underlying molecular mechanism of its cellular toxicity. The role of dissolution in the toxicity of ZnO nanoparticles was also investigated. Our results demonstrate that HepG2 cells exposed to 14–20 μg/ml ZnO nanoparticles for 12 h showed a decrease in cell viability and the mode of cell death induced by ZnO nanoparticles was apoptosis. They also induced DNA damage which was mediated by oxidative stress as evidenced by an increase in Fpg sensitive sites. Reactive oxygen species triggered a decrease in mitochondria membrane potential and an increase in the ratio of Bax/Bcl2 leading to mitochondria mediated pathway involved in apoptosis. In addition, ZnO nanoparticles activated JNK, p38 and induced p53 Ser15 phosphorylation. However, apoptosis was found to be independent of JNK and p38 pathways. This study investigating the effects of ZnO nanoparticles in human liver cells has provided valuable insights into the mechanism of toxicity induced by ZnO nanoparticles.
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1Apoptosis
2Apoptosis - drug effects
3Apoptosis Regulatory Proteins - metabolism
4Biochemistry
5Biomedical and Life Sciences
6Biomedicine
7Cancer Research
8Cell Biology
9Cell death
10Cell Survival - drug effects
11Cells
12DNA
13DNA Damage
14Enzyme Inhibitors - pharmacology
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17Humans
18L-Lactate Dehydrogenase - metabolism
19Lipid Peroxidation
20Membrane Potential, Mitochondrial
21Mitochondria, Liver - drug effects
22Mitochondria, Liver - metabolism
23Mitochondrial DNA
24Mitogen-Activated Protein Kinases - antagonists & inhibitors
25Mitogen-Activated Protein Kinases - metabolism
26Mutagens - toxicity
27Nanoparticles
28Nanoparticles - toxicity
29Nanoparticles - ultrastructure
30Nanotechnology
31Oncology
32Original Paper
33Oxidation-Reduction
34Oxidative Stress
35Particle Size
36Phosphorylation
37Physiological aspects
38Protein Processing, Post-Translational
39Reactive Oxygen Species - metabolism
40Tumor proteins
41Virology
42Zinc oxide
43Zinc Oxide - metabolism
44Zinc Oxide - pharmacology
45Zinc Oxide - toxicity
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abstractThe wide scale use of Zinc oxide (ZnO) nanoparticles in the world consumer market makes human beings more prone to the exposure to ZnO nanoparticles and its adverse effects. The liver, which is the primary organ of metabolism, might act as a major target organ for ZnO nanoparticles after they gain entry into the body through any of the possible routes. Therefore, the aim of the present study was to assess the apoptotic and genotoxic potential of ZnO nanoparticles in human liver cells (HepG2) and the underlying molecular mechanism of its cellular toxicity. The role of dissolution in the toxicity of ZnO nanoparticles was also investigated. Our results demonstrate that HepG2 cells exposed to 14–20 μg/ml ZnO nanoparticles for 12 h showed a decrease in cell viability and the mode of cell death induced by ZnO nanoparticles was apoptosis. They also induced DNA damage which was mediated by oxidative stress as evidenced by an increase in Fpg sensitive sites. Reactive oxygen species triggered a decrease in mitochondria membrane potential and an increase in the ratio of Bax/Bcl2 leading to mitochondria mediated pathway involved in apoptosis. In addition, ZnO nanoparticles activated JNK, p38 and induced p53 Ser15 phosphorylation. However, apoptosis was found to be independent of JNK and p38 pathways. This study investigating the effects of ZnO nanoparticles in human liver cells has provided valuable insights into the mechanism of toxicity induced by ZnO nanoparticles.
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pmid22395444
doi10.1007/s10495-012-0705-6