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ANTI-AGEING EFFECTS OF SELENIUM 

http://www.chemsoc.org/exemplarchem/entries/2003/imperial_Burgoine/origins.txt.html

Evolutionary considerations suggest that ageing is caused not by active gene programming but by evolved limitations in cellular maintenance, resulting in a gradual accumulation of damage.  A complex array of systems and mechanisms operate to limit this damage (Kirkwood, 2005), and Se plays important roles in several of these.  In addition to Se’s life-extending effects through its general antioxidant, immune system and endocrine functions, it appears to have specific anti-ageing effects in cells, which operate at the DNA level. 

Mitochondria, the energy-producing organelles which can number in the thousands per cell, are, because of their main respiratory function, subjected to higher levels of oxidative stress than other sub-cellular sites.  Moreover, mitochondrial DNA is less stable than nuclear DNA.  Degeneration in mitochondria is known to be an important factor in ageing, and is largely a consequence of accumulation of mitochondrial DNA mutations.  Older individuals have lower mitochondrial membrane potential, cellular oxygen consumption, cardiolipin levels and respiratory control ratio (Ames, 1998).  Furthermore, abundance of functional mitochondrial DNA is associated with ATP production rate, aerobic capacity and glucose tolerance (Short et al, 2005).

Certain antioxidants, amino acids, enzymes, coenzymes and thiols have been shown to be particularly important in preserving mitochondrial integrity.  These include Se, vitamin E, L-carnitine, alpha-lipoic acid and coenzyme Q10.  For example, a recent study found that a combination of L-carnitine and alpha-lipoic acid reversed the age-associated decline in mitochondrial enzyme activity, and thereby protected the mitochondria from ageing (Savitha et al, 2005).  Activity of Se-dependent glutathione peroxidase in mitochondria increases with age in healthy mammals, in order to counter the increased oxidative stress associated with ageing (Nohl et al, 1979).  Furthermore, it is well known that caloric restriction has both anti-cancer and anti-ageing effects in experimental animals.  Sanz et al (2005) found that caloric restriction decreases ageing rate, in part, by lowering the rate of free radical generation of mitochondria in the brain.

Another anti-ageing effect of Selenium is maintaining the length of telomeres at the ends of nuclear chromosomes.  With each cell division, telomeres shorten, eventually leading to cell death and consequent tissue ageing.  This effect can be delayed by maintenance of telomere length.  Chinese researchers found that selenium at relatively low doses maintained telomere length in cultured liver cells by increasing the activity of telomerase, the enzyme involved in telomere synthesis.  Lead acetate on the other hand “remarkably shortened” the telomere length in these cells Liu et al, 2003; 2004).  

Definitions

Mitochondria: the “powerhouses of the cell”, which produce adenosine triphosphate (ATP), the “energy currency” of the cell, through the metabolism of pyruvic acid and other energy-containing molecules.

Telomere: a special DNA sequence at the tip of a chromosome, which is essential for chromosome stability. In the absence of a mechanism for adding more telomere (such as the enzyme telomerase), telomeres erode slightly with each cell division.

Telomerase: An enzyme complex composed of an RNA subunit attached to protein. Telomerase is a reverse transcriptase that, when active, adds telomere to the ends of chromosomes.

Alpha-lipoic acid: a sulphur-containing fatty acid (thiol) which is an important component of coenzymes involved in biological oxidation and reduction.  It is important in protein, fat and carbohydrate metabolism.

L-carnitine: formed from the two essential amino acids lysine and methionine.  It facilitates the transport of fatty acids within cells to sites where they are oxidised.

Coenzyme Q10 (ubiquinone): a fat-soluble electron carrier that operates in the electron transport (respiratory) chain in mitochondria.

References

Ames, BN 1998. Micronutrients prevent cancer and aging. Toxicol Lett 28(102-103): 5-18.

Kirkwood TB 2005. Understanding the odd science of aging. Cell 120(4): 437-447.

Liu Q, Wang H, Hu DC, Ding CJ, Xiao H, Xu HB, Shu BH, Xu SQ 2003. Effects of selenite on telomerase activity and telomere length. Sheng Wu Hua Xue Yu Sheng Wu Wu Li Xue Bao (Shanghai) 35(12): 1117-1122. 

Liu Q, Wang H, Hu D, Ding C, Xu H, Tao D 2004. Effects of trace elements on the telomere lengths of hepatocytes L-02 and hepatoma cells SMMC-7721. Biol Trace Elem Res 100(3): 215-228.

Nohl H, Hegner D, Summer KH 1979. Responses of mitochondrial superoxide dismutase, catalase and glutathione peroxidase to aging. Mech Ageing Dev 11(3): 145-151.

Sanz A, Caro P, Ibanez J, Gomez J, Gredilla R, Barja G 2005. Dietary restriction at old age lowers mitochondrial oxygen radical production and leak at complex I and oxidative DNA damage in rat brain. J Bioenerg Biomembr 37(2): 83-90.

Savitha S, Tamilselvan J, Anusuyadevi M, Panneerselvam C 2005. Oxidative stress on mitochondrial antioxidant defense system in the aging process: role of DL-alpha-lipoic acid and L-carnitine. Clin Chim Acta 355(1-2): 173-180.

Short KR, Bigelow ML, Kahl J, Singh R, Coenen-Schimke J, Raghavakaimal S, Nair KS 2005. Decline in skeletal muscle mitochondrial function with aging in humans. Proc Natl Acad Sci USA 102(15): 5618-5623.

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