Carnosine rejuvenates the skin
The replication capability of cells also undergoes the aging process. In each division, DNA telomeres shorten. Telomeres are the repeating marginal DNA sequences that protect the chromosomes. The DNA shortening after each division causes, at some point, the formation of DNA - damage signals, which then activates p53. Some chemotherapeutics accelerate the aging process in both malignant and healthy cells.. Carnosine, on the other hand, has a very effective impact on reversing the aging signs in skin cells (fibroblasts) firstly in the aging process and also in renewing their functionality which together help in prolonging their lifetime.
These functions are characteristic carnosine effects of preventing the creation of all kinds of harmful changes in protein and phospholipid molecules, but also, and very significantly, the capability of carnosine to reduce telomere shortening and inhibit DNA damage. The Hayflick limit or Hayflick phenomenon is the number of times a normal human cell population will divide before cell division stops. The Hayflick limit therefore refers to cell mortality. Most of the cells actually regenerate by dividing into two daughter cells. Dr. Hayflick in 1961 proved, that cells are able to reach a certain number of divisions and lose the ability to divide afterwards. His famous experiments have proven that the cells in human fibroblast cultures are able to divide up to 60- 80 times, while young people fibroblasts were able to divide 30 - 40 times and elderly fibroblasts 10 to 20 times. Cell senescence (aging) begins when the cell reaches Hayflick limit. The cells in senescence are still alive, but they do not divide any further and structural and functional damage can be found. Human fibroblasts are very suitable for carrying out the experimental laboratory studies, because senescent fibroblast cultures cannot be confused with young ones with characteristic uniformity and parallel fibre groups formations. On the contrary, senescent fibroblasts are of a granular nature, do not form groups and their fibres are irregular and different in length - they have lost the ability to organize regular forms. These significant characteristics of old cells are called senescent phenotype (the young cells have juvenile phenotype)
Australian scientists of Dr. MacFarland's team realized an interesting study, which proved that carnosine rejuvenates the cells close to senescence. The most exciting fact in their experiment is that the ability of carnosine to reverse the signs of aging was proven. When the aging cells were inserted into the carnosine enriched culture, they demonstrated not only phenotype change (senescent to juvenile) but also an increased ability to divide. They manifested the ability to organize again, became uniform and formed organized fibre groups. When moved back to the culture without carnosine, signs of senescence reappeared quickly. The same cells were again moved to the carnosine culture where they manifested juvenile phenotypes again. This was repeated many times with the same cells with the same result - cells in carnosine culture had juvenile phenotype and without carnosine showed senescent phenotype. Moreover, carnosine significantly prolonged the lifetime of old cells. These experiments were later confirmed by Dr. Alan Hipkis, mainly the ability to prolong the lifetime of human fibroblasts. Carnosine delays the aging processes in human fibroblasts cultures and changes senescent phenotype to juvenile. Anyhow the antioxidants show positive properties in the removal of free radicals, they cannot illustrate the properties against aging like carnosine. Especially the associated, special effects of carnosine are its attributes in the senescence process. Carnosine in particular is able to react with protein carbonyl groups forming “carnosinylated” polypeptide adducts - these suppress aging and restrict the formation of damaged proteins.
The revitalizing effect of carnosine on fibroasts explains why carnosine significantly improves wound healing after surgery.
What causes wrinkles? Aging (senescent) skin cells, keratinocytes and fibroblasts, by means of protein molecules, begin to “behave” abnormally and accumulate in the human skin over time. They produce more metalloproteinase enzymes that destroy proteins in the surrounding extracellular matrix (where cells, lymph nodes, blood veins and skin structures are embedded. They also produce adhesive molecules causing thickening and calcifying of artery walls - arteriosclerosis. Senescent cells produce more degrading enzymes and pro-inflammatory cytokines with the effects in distant areas of the body (blood transport). Thereby a relatively small amount of senescent cells cause quite extensive skin function and integrity changes. Senescent cells also accumulate with age in all organs and tissues, resisting apoptosis and causing degenerative aging processes. Additionally, by the disruption of the microscopic environment, senescent cells can accumulate and be one of the prevalent reasons of malignant diseases in the elderly.
