Friday, May 11, 2012

Advances in carcinogenic metal toxicity and potential molecular markers. (1 of x in a series)

Well, this is a very interesting article indeed.  This weekend, i am going to re read and publish the oxidative stress issues that have been reviewed in a number of journal articles re the hip artheroplasties.  I will also present these articles to the oncologists I will be seeing over the next two weeks at the top 3 cancer centers for my own condition that has developed.
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Int J Mol Sci. 2011;12(12):9576-95. Epub 2011 Dec 20.

Advances in carcinogenic metal toxicity and potential molecular markers.

Source

Department of Life Science, Dongguk University, 30 Pildong-ro 1-gil (26 Pildong 3-ga), Jung-gu, Seoul 100-715, Korea; E-Mail: pkoedrith@gmail.com.

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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