**7. Conclusion**

Furthermore, some RNA viruses, as well as leader mRNAs contain RNA-like segments that may interact with specific enzymes and, thus, play regulatory roles [99]. Hence, it is reasonable to assume that detailed information concerning selenium-modified RNAs may contribute to the understanding of the biological roles of selenium [100]. Near toxic levels of selenium have been reported to produce tumours in rats but other studies indicated that these concentrations

In mammals glutathione peroxidase is the only selenium-dependent enzyme so far identified, but it seems unlikely that the complicated biological effects of selenium in man and animals are attributable solely to variations in the level of this enzyme. In fact, at least two other seleno proteins of unknown catalytic activity have been detected in animals. Investigations in a variety of animal systems have suggested that there is a significant interaction of selenium with glutathione independent of the enzyme glutathione peroxidase [101]. White muscle disease (WMD), a degenerative muscle disease, found in domestic animals [102, 103]. It is caused by a deficiency of selenium and/or vitamin E. Selenium and vitamin E deficiencies can produce symptoms of ill thrift and reproductive losses: lower conception rates, fetal reabsorp‐ tion, dystocia, retained placenta, reduced milk production, and reduced semen quality, poor rate of growth or ill thrift in young lambs, low wool yields and have increased incidence of periodontal disease [102, 103]. Selenium appears to be a key nutrient in counteracting the development of virulence and inhibition of HIV progression to AIDS. It is required for sperm motility and may reduce the risk of miscarriage. Selenium deficiency has been linked to adverse mood states and some findings suggest that selenium deficiency may be a risk factor in cardiovascular diseases [104]. Studies continue to confirm that people with higher levels of

of selenium created chronic toxic hepatitis that resembled hyperplasia.

302 Pharmacology and Nutritional Intervention in the Treatment of Disease

selenium in their blood have lower rates of prostate and lung cancers [105].

organic hydroperoxides [107].

melanoma, among women but not among men [113].

Selenium is synergistic with vitamin E; they serve related metabolic functions and share in common the role of endogenous antioxidants [106]. Vitamin E has a free radical Scavenger, and Se as a component of the peroxide reducing enzyme, glutathione peroxidase. Vitamin E restricts the formation of peroxides by neutralizing free radicals, an integral component of glutathione peroxidase, an enzyme responsible for the removal of hydrogen peroxide and

Selenium and vitamin C; CH3SeH is thought to be a critical metabolite in Se chemoprevention [108, 109]. The family of selenoenzymes called thioredoxin reductases catalyze the NADPHdependent reduction of oxidized thioredoxin, hyperoxides, dehydroascorbate, ubiquinol and other substrates [110].The action of thioredoxin reductases in recycling dehydroascorbate to ascorbate (vitamin C) now explain the synergistic action of selenium and vitamin C [111]. The thioredoxin system is also capable of regenerating proteins inactivated by ROS. Daily supple‐ mentation with vitamin C (120 mg), vitamin E (30 mg), beta-carotene (6 mg), and the minerals selenium (100 µg) and zinc (20 mg) for a median of 7.5 years had no effect on the incidence of cancer or cardiovascular disease or on all-cause mortality [112]. Antioxidant and mineral supplementation was associated with lower total cancer incidence and all-cause mortality among men but not among women, and with an increase in skin cancer incidence, including

Selenium and Silver; Selenium serves as a major protective factor in precipitating the silver in a highly insoluble and hence inert form of silver selenide. Although some of this may be taken

Selenium as non-metals is an essential nutrient that acts as cofactor in enzyme oxidation– reduction reactions. It maintains the specific configurations of proteins, is incorporated into the structure of hormones, and plays a structural and catalytic role in gene expression and transcriptional regulation. In the physiological dosage range, Se appears to function as an antimutagenic agent, preventing the malignant transformation of normal cells and the activation of oncogenes. These protective effects of Se seem to be primarily associated with its presence in the glutathione peroxidases, which are known to protect DNA and other cellular components from damage by oxygen radicals. Selenoenzymes are also known to play roles in carcinogen metabolism, in the control of cell division, oxygen metabolism, detoxification processes, apoptosis induction and the functioning of the immune system. Other modes of action, either direct or indirect, may also be operative, such as the partial retransformation of tumor cells and the inactivation of oncogenes.
