Monday, June 17, 2024
Mitochondrial Health

skinactives.com – Mitochondria and aging – Part 1



Skin Actives is proud to launch our most exciting product ever plant mitochondria concentrate. Up to now skin care products have been designed to repair existing mitochondria, our new active takes a massive step beyond that with a completely new technology that provides mitochondrial spare parts to the skin.

Dr. Sivak has also formulated a new mitochondrial booster cream with the mitochondria concentrate.

Concentrate Link: http://www.skinactives.com/product/detail.aspx?prodID=167
Cream Link: http://www.skinactives.com/product/detail.aspx?prodID=168

Need ATP? Get spare parts for your skin mitochondria at SAS!

Mitochondria (sing. mitochondrion, from the Greek mitos, warp thread + Greek khondrion, diminutive of khondros, grain, granule).

Mitochondria provide the energy as adenosine triphosphate (ATP), the form of energy our cells can use to do housekeeping, grow and divide. This is true not just for us, humans, but for all eukaryotes (organisms with nuclei). Mitochondria use molecular oxygen to extract a lot of energy that would otherwise be lost, and foodstuff is eventually converted to low energy water and carbon dioxide.

This great energy-converting efficiency comes at a cost: mitochondria produce strong oxidants like hydrogen peroxide and the superoxide and hydroxyl radicals as by-products. All of the cell sophisticated antioxidant mechanisms (including vitamin C, glutathione and vitamin E) cant completely protect mitochondria from slow but persistent damage. This oxidative stress makes mitochondria age at a faster pace than the rest of the cell, because oxidation of lipids, proteins, RNA, and DNA is faster. Indeed, oxidative damage to mitochondrial DNA (the only organelle with its own DNA outside the nucleus) is 8 to 10-fold higher than the damage found in nuclear DNA. Oxidative damage also affects adversely the inner mitochondrial membrane, where the crucial enzyme ATPase is located and where ATP is produced. The phospholipids of the inner mitochondrial membrane change and become even more sensitive to oxidative damage. These changes are bound to affect membrane fluidity and permeability and will certainly impair the ability of mitochondria to meet cellular energy demands.

This oxidant-induced acceleration of senescence has major consequences for mitochondria: aging mitochondria lose efficiency in their job of extracting the last bit of energy from foodstuff: enzyme activity and substrate binding affinity decrease. This decay in function can be partially reversed in aged animals by feeding them the mitochondrial metabolites acetyl carnitine and lipoic acid, and information of this sort provides circumstantial evidence for the mitochondrial theory of aging (a.k.a. free radical theory of aging) which states that the slow accumulation of impaired mitochondria is the driving force of the aging process.

Even if we dont accept the theory that mitochondrial aging is the cause of overall aging, there is no doubt that deterioration of mitochondria is at least responsible for the aging of the whole organism. Up to now, this information has been translated into the topical application of alpha lipoic acid, acetyl carnitine and various antioxidants in anti-age skin care products.

We at SAS take the effect of oxidants on the cell very seriously: we have been offering acetyl carnitine and alpha lipoic acid both as pure chemicals and in ready-to-use skin care products. We also broadened the spectrum of antioxidants (see for example antiOx booster, CHAS serum) and lipids (ELS serum) for the prevention and reversal of skin damage. Addition of mitochondrial concentrate to our actives and ready mixed products is a natural step in the efforts of Skin Actives Scientific to bring the benefits of scientific knowledge and technology to our clients.

References: Harman, D. (1983). Free radical theory of aging: consequences of mitochondrial aging. Age 6:8694.

Hampton, T. (2005) Study reveals mitochondrial role in aging. JAMA, 294:672.

Liu, J., Atamna, H Kuratsune, H., Ames, BN. (2002) Delaying brain mitochondrial decay and aging with mitochondrial antioxidants and metabolites Ann N Y Acad Sci, 959: 133-66.

See also http://en.wikipedia.org/wiki/Mitochondria

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