Document Detail

The role of nickel and nickel-mediated reactive oxygen species in the mechanism of nickel carcinogenesis.
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MedLine Citation:
PMID:  7843115     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Increasing evidence demonstrates the reactive oxygen species (ROS) are implicated in metal carcinogenesis. Exposure of cultured Chinese hamster ovary (CHO) cells to several nickel compounds, i.e. NiS, Ni3S2, NiO (black and green), and NiCl2 has been shown to increase oxidation of 2',7-dichlorofluorescein to the fluorescent 2',7-dichlorofluorescein (DCF), suggesting that nickel compounds increased the concentration of oxidants in CHO cells. This fluorescence can be attenuated by addition of exogenous catalase to the extracellular media, indicating that H2O2 is one of the formed oxidants in this system. Fluorimetric measurements of chromogens following thiobarbituric acid reaction showed that nickel compounds also induce lipid peroxidation with a decreasing potency NiS, Ni3S2 > black NiO > green NiO > NiCl2. These results suggest that lipid hydroperoxides may also be produced through the action of nickel in intact cells. MgCl2, an antagonist of Ni-induced DNA strand breaks and cell transformation, has no effect on the formation of DCF fluorescence induced in CHO cells by nickel. The results suggest that nickel is an active inducer of ROS in intact mammalian cells and that the molecular mechanism of nickel carcinogenesis may involve multiple steps of nickel-mediated ROS.
Authors:
X Huang; Z Zhuang; K Frenkel; C B Klein; M Costa
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Environmental health perspectives     Volume:  102 Suppl 3     ISSN:  0091-6765     ISO Abbreviation:  Environ. Health Perspect.     Publication Date:  1994 Sep 
Date Detail:
Created Date:  1995-03-08     Completed Date:  1995-03-08     Revised Date:  2009-11-18    
Medline Journal Info:
Nlm Unique ID:  0330411     Medline TA:  Environ Health Perspect     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  281-4     Citation Subset:  IM    
Affiliation:
Nelson Institute of Environmental Medicine, New York University Medical Center, New York.
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MeSH Terms
Descriptor/Qualifier:
Animals
CHO Cells
Carcinogens / metabolism*
Catalase / pharmacology*
Cricetinae
Fluoresceins / metabolism
Lipid Peroxidation / drug effects
Magnesium Chloride / pharmacology*
Nickel / toxicity*
Oxidation-Reduction
Reactive Oxygen Species / metabolism*
Grant Support
ID/Acronym/Agency:
ES 04712/ES/NIEHS NIH HHS; ES 04895/ES/NIEHS NIH HHS; ES 05512/ES/NIEHS NIH HHS
Chemical
Reg. No./Substance:
0/Carcinogens; 0/Fluoresceins; 0/Reactive Oxygen Species; 1313-99-1/nickel monoxide; 16812-54-7/nickel sulfide; 7440-02-0/Nickel; 76-54-0/2',7'-dichlorofluorescein; 7718-54-9/nickel chloride; 7786-30-3/Magnesium Chloride; EC 1.11.1.6/Catalase
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Full Text
Journal Information
Journal ID (nlm-ta): Environ Health Perspect
ISSN: 0091-6765
Article Information
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Print publication date: Month: 9 Year: 1994
Volume: 102 Issue: Suppl 3
First Page: 281 Last Page: 284
ID: 1567368
PubMed Id: 7843115

The role of nickel and nickel-mediated reactive oxygen species in the mechanism of nickel carcinogenesis.
X Huang
Z Zhuang
K Frenkel
C B Klein
M Costa
Nelson Institute of Environmental Medicine, New York University Medical Center, New York.



Article Categories:
  • Research Article


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