|
KMID : 1140120090140040292
|
|
Cancer Prevention Research
2009 Volume.14 No. 4 p.292 ~ p.296
|
|
|
Overview on the Mechanism of Molecular Toxicity Induced by Nickel Exposure
|
|
Lee Sang-Min
Choi Nam-Woo
Hwang Seung-Yong
Seo Young-Rok
|
|
|
Abstract
|
|
|
|
Nickel (Ni) is a widely distributed industrial metal which can expose to human through polluted environments including nickel refining, electroplating, and welding industries. Ni exposure can cause a variety of pathological cellular effects through generation of reactive oxygen species (ROS), genotoxicity, inhibition of Ni-binding proteins, dysregulation of cell cycle control and apoptosis and DNA repair inhibition. Ni-induced ROS can lead to DNA damage, which can produce 8-oxo-dG, and triggers cell signaling pathways involve in cellular proliferation, apoptosis, and transformation. Furthermore, accumulation of nickel into the cells has negative impact on genetic materials, particularly on chromosome, resulting in chromosomal deletion, aberration, and regional decondensation. Nickel compounds also modulate gene expression including c-myc, proto-oncogene whose product play role in carcinogenesis. Recent studies have shown that many proteins with strong affinity to Ni are involved in nickel transport, detoxification and excretion. Moreover, binding ability of Ni to particular proteins crucial for cellular functioning raises the possibility to change in homeostasis. Of interest, inhibition of DNA repair by nickel compounds probably causes cell death and mutation. The present review will provide information on the molecular and cellular toxicity of heavy metal nickel as one of most concerning environmental carcinogens.
|
|
|
KEYWORD
|
|
|
ROS, Genotoxicity, DNA repair
|
|
|
FullTexts / Linksout information
|
|
|
|
|
|
Listed journal information
|
|
 
|
|