**1. Introduction**

[17] Adewole SO, Salako AA, Doherty OW, Naicker T (2007). Effect of melatonin on car‐ bon tetrachloride-induced kidney injury in Wistar rats. Afr*. J. Biomed*. *Res.,* 10:

[18] Arun K and Balasubramanian U (2011).Comapartive study on hepatoprotective ac‐ tivity of *phyllanthus amarus* and *eclipta prostrata* against alcohol induced in albino rats.

[19] Gnanadesigan M, Ananad M, Ravikumar S, Maruthupandy M, Syed Ali M, Vijaya‐ kumar V, Kumaraguru AK (2011).Antibacterial potential of biosynthesized silver

[21] Krithika R and VERMA R J (2009). Ameliorative potential of phyllanthus amarus against carbon tetrachloride-induced hepatotoxicity. Acta Poloniae Pharmaceutica ñ

[22] Snedecor GW, Cochran, WG (1989).Statistical method.8th edition Ames,IA:Affiliated

[23] Rajeshkumar NV, Joy KL, Kuttan G, Ramsewak RS, Nair MG, Kuttan R (2002). Anti‐ tumour and anticarcinogenic activity of Phyllanthus amarus extract. J Ethnopharma‐

[24] Narah M, Kalita JC, Kotoky J (2012). Medicinal plants with potential anticancer activ‐

ities: a review. International Research Journal of Pharmacy.3 (6)

nanoparticles using *Avicennia marina* mangrove plant, Applied Nanoscience.

International journal of environmental sciences volume 2:1.

[20] Gao H, Zhou YW (2005).World. J. Gastroenterol.11, 3671.

Drug Research, 66(5)-579-583.

294 Pharmacology and Nutritional Intervention in the Treatment of Disease

east-West Press;217-36.

col.81(1):17-22.

153-164.

Cancer is the leading cause of death in economically developed countries and the second leading cause of death in developing countries (WHO)1 . It is extraordinarily complex with novel mutations and phenotypes that are often unique to an individual. It is a disease of the chromosomes and the problem is, in almost all cancers, it isn't just one mutation but may be much more. Cancer may be regarded as a complex metabolic deficiency disease [9, 10, 11, 12, 13, 14]

Cancer diet is also used as a complementary approach to cancer that involves the use of special nutritional supplements. Selenium (Se) and cancer is a term that can be referred to the approach or associations between cancer and nutrition that is to lower an individual's risk of cancer. Selenium was first recognized as having some nutritional importance almost six decades ago [15]. Selenium is found in food as selenoamino acids or selenoproteins, and as selenide, selenite, or selenate [16]. Selenium is a critical cofactor in the activity of gluthathione peroxidase and is also important in the management of peroxynitrite. The selenium content of food depends upon soil content and varies regionally and nationally, with soil levels relatively low in most European countries [17, 18, 19]. Soil conditions have been associated with clinical selenium toxicity in animals (selenosis) in some areas with very high selenium content, and with selenium deficiency syndromes in animals and humans in areas of low soil selenium [17].

Selenium is essential nutrient that act as cofactor in enzyme oxidation–reduction reactions (e.g. iodothyronine deiodinase and glutathione peroxidases) [20]. It maintains the specific config‐ uration of proteins, is incorporated into the structure of hormones, and plays a structural and catalytic role in gene expression and transcriptional regulation. The trace element selenium is contained in soil and drinking water varies from area to area, which determines the variation in intake seen in different communities and the amount and chemistry of dietary constituents

© 2014 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

eaten with the this element affect the absorption efficiency of the selenium is said be 'the only trace element to be specified in the genetic code' [21].

of redox signalling, redox being a term used for reduction and oxidation. Healthy cells and also malignant ones benefit from intact Keap1/Nrf2 signalling, making a dysregulated hydroperoxide signaling a plausible explanation for the increased cancer risk in selenium deficiency [42]. Therefore, a research agenda to investigate the synergistic operation of such

The Pharmacology and Biochemistry of Selenium in Cancer

http://dx.doi.org/10.5772/58425

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Cancer is a generic term for a large group of diseases that can affect any part of the body and it can exist in many different forms and types, some of which are brought on by the destructive choices people make while others are less predictable and are not the result of destructive decisions. It can be broadly grouped into different types (Carcinomas, Sarcomas, Lymphomas and Leukaemia's), depending on which tissues they come from [43, 44]. Cancer develops when cells multiply in the presence of oxidation and other damage. According to micro-evolutionary models, cells become damaged and change their behaviour, growing uncontrollably, and act like the single-celled organisms from which they originally evolved. The cancer cells' indi‐ vidualism overwhelms the cooperative control processes that are essential to a complex multicellular organism [45, 46]. As cancers become malignant, they exhibit incredible genetic diversity. Whereas a benign tumour is like a colony of similar abnormal cells, a malignant tumour is a whole ecosystem. At this late stage, some (but not all) antioxidants can indeed promote cancer cell growth. Thousands of different cell types coexist: cooperating, competing, and struggling to survive. A consequence of the anaerobic conditions that prevail during the early development of a malignancy is that cancer cells differ from healthy cells, in that they have been selected for the way they generate energy (i.e. anaerobically, using glucose) [47, 48].

The sulfhydryl group is the most sensitive to the oxidizing effects of ROS among the amino acid side chains in protein; it is often involved in the intracellular transduction machinery of redox signals in response to physiological and oxidative stimuli. In fact, a variety of biological functions, not directly related to peroxidase activity, have also been reported for the Prx family [49]. Oxidative damage in DNA can cause cancer. Several antioxidant enzymes such as superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, glutathione Stransferase etc. protect DNA from oxidative stress. It has been proposed that polymorphisms in these enzymes are associated with DNA damage and subsequently the individual's risk of

Nutrition and physical activity and major lifestyle changes can reduce the risk of cancer [51, 52]. Antioxidants are becoming an increasingly common choice as a hopeful cancer prevention agent. Importantly, antioxidants limit oxidative damage and thus inhibit early benign cancer growth, preventing cancer from developing. Selenium has received publicity over the past decades based on some confusing and contradictory research about whether low-selenium diets are implicated in cancer risk. To date, this is still a question without a clear answer. However, selenium is required for the proper activity of a group of enzymes collectively called glutathione peroxidase. Each of these enzymes helps to turn toxic hydrogen peroxide into

substances in cancer treatment is required.

**3. Cancer and oxidation**

cancer susceptibility [50].

Selenocysteine is a vital component of 35 or more selenoproteins, some of which are important enzymes [22]. Selenium functions as a redox centre, an example of which is the reduction of hydrogen peroxide and lipid and phospholipid hydroperoxides to nondamaging water and alcohols by the glutathione peroxidases [23]. Functions of this kind help maintain membrane integrity, and protect prostacyclin production. Prevention of the oxidative chain reactions in this way prevents further damage to lipids, lipoproteins, and DNA; hence its antioxidant function helps prevent atheroma and cancer, among other things [24, 25, 26].
