Publication: Advances in Carcinogenic Metal Toxicity and Potential Molecular Markers
Accepted Date
2011-12-12
Issued Date
2011-12
Resource Type
Language
eng
ISSN
1422-0067
Rights
Mahidol University.
Bibliographic Citation
International Journal of Molecular Sciences. Vol. 12, No.12 (2011), 9576-9595.
Suggested Citation
Preeyaporn Koedrith, Young Rok Seo, Koedrith, Preeyaporn, Koedrith, P., ปรียาพร เกิดฤทธิ์ Advances in Carcinogenic Metal Toxicity and Potential Molecular Markers. International Journal of Molecular Sciences. Vol. 12, No.12 (2011), 9576-9595.. doi:10.3390/ijms12129576 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/48737
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Title
Advances in Carcinogenic Metal Toxicity and Potential Molecular Markers
Abstract
Metal compounds such as arsenic, cadmium, chromium, cobalt, lead, mercury,
and nickel are classified as carcinogens affecting human health through occupational
and environmental exposure. However, the underlying mechanisms involved in tumor
formation are not well clarified. Interference of metal homeostasis may result in oxidative
stress which represents an imbalance between production of free radicals and the system’s
ability to readily detoxify reactive intermediates. This event consequently causes DNA
damage, lipid peroxidation, protein modification, and possibly symptomatic effects for
various diseases including cancer. This review discusses predominant modes of action and
numerous molecular markers. Attention is paid to metal-induced generation of free radicals,
the phenomenon of oxidative stress, damage to DNA, lipid, and proteins, responsive signal
transduction pathways with major roles in cell growth and development, and roles of
antioxidant enzymatic and DNA repair systems. Interaction of non-enzymatic antioxidants
(carotenoids, flavonoids, glutathione, selenium, vitamin C, vitamin E, and others) with
cellular oxidative stress markers (catalase, glutathione peroxidase, and superoxide
dismutase) as well as certain regulatory factors, including AP-1, NF-κB, Ref-1, and p53 is
also reviewed. Dysregulation of protective pathways, including cellular antioxidant
network against free radicals as well as DNA repair deficiency is related
to oncogenic stimulation. These observations provide evidence that emerging oxidative stress-responsive regulatory factors and DNA repair proteins are putative predictive factors
for tumor initiation and progression.
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