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Vitamin E delays progression of cellular senescence

Tuesday, December 8, 2015

An article appearing this year in BioMed Research International reveals new findings concerning the antiaging properties of vitamin E. In an experiment involving two types of human cells, treatment with vitamin E resulted in a delay in cellular senescence in comparison with untreated cells.

Senescent cells are those that have reached a state of irreversible growth arrest by attaining a limited number of divisions. According to authors Giorgio La Fata and colleagues, cellular senescence in vitro is related to the aging of organisms in vivo.

"An important contributor to the development of the senescence process is oxidative stress," Dr Fata and coauthors note. "Oxidative stress usually occurs when the production or the exposure to reactive oxygen species (ROS) overwhelms the antioxidant systems of the cells."

"Vitamins E and C are important natural antioxidants capable of neutralizing the deleterious effects of ROS," they observe.

The team tested the effects of vitamin E in cultured human umbilical vein endothelial cells and human fibroblast cells. Senescence was assessed by periodic measurement of the number of cells that expressed the enzyme marker beta-galactosidase.

The researchers found an increase in the number of beta-galactosidase-positive cells over time in both types of cells; however, short-term vitamin E supplementation was associated with a reduction in the percentage of positive (senescent) cells in comparison with untreated control cells. Longer term vitamin E treatment of human umbilical vein endothelial cells was found to be associated with an eventual reduction in cellular proliferation, which suggests that chronic vitamin E treatment decreases the number of senescent cells by reducing their proliferative capacity. The researchers determined that the vitamin acts through the downregulation of the overexpression of the P21 gene.

"Our data demonstrate that through specific micronutrient supplementation it is possible to delay the onset of cellular senescence in two in vitro models: human endothelial cells and fibroblasts," Dr La Fata and associates conclude. "Additional research is needed to identify the mechanisms that drive and regulate cellular senescence and to identify specific pathways that can be regulated by supplementation with particular micronutrients."

 
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Quercetin among new class of treatments for aging identified
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A new class of drugs labeled senolytics that may combat some of the factors associated with aging has been identified by researchers at the Scripps Research Institute. Senescent cells are those which have stopped dividing, and their accumulation has been associated with accelerated aging.

In an article published in the August 2015 issue of Aging Cell, Paul Robbins, PhD, and colleagues document their discovery of increased expression of pro-survival networks in senescent cells. Compounds that target these networks, dubbed senolytics, include the drug dasatinib and the nutrient quercetin, which is found in fruits and vegetables, and is also available as a nutritional supplement. While dasatinib was found to reduce senescent human fat cell progenitors, quercetin showed a greater effect against senescent human endothelial cells and mouse bone marrow mesenchymal stem cells. The combination of both compounds was shown to eliminate senescent mouse embryonic fibroblasts.

"We view this study as a big, first step toward developing treatments that can be given safely to patients to extend healthspan or to treat age-related diseases and disorders," stated Dr Robbins. "When senolytic agents, like the combination we identified, are used clinically, the results could be transformative."

"In animal models, the compounds improved cardiovascular function and exercise endurance, reduced osteoporosis and frailty, and extended healthspan," reported research team member Laura J. Niedernhofer. "Remarkably, in some cases, these drugs did so with only a single course of treatment."

"Senescence is involved in a number of diseases and pathologies so there could be any number of applications for these and similar compounds," Dr Robbins added. "Also, we anticipate that treatment with senolytic drugs to clear damaged cells would be infrequent, reducing the chance of side effects."

 
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Prevention

The results of tens of thousands of scientific studies make it abundantly clear that following the proper lifestyle can add a significant number of healthy years to the average person's lifespan.

The premise of taking action to maintain youthful health and vigor is based on findings from peer-reviewed scientific studies that identify specific factors that cause us to develop degenerative disease. These studies suggest that the consumption of certain foods, food extracts, hormones, or drugs will help prevent common diseases associated with normal aging.

One of the most compelling reports that high-potency supplements extend lifespan in humans was in the August 1996 issue of the American Journal of Clinical Nutrition. This study involving 11 178 elderly people attempted to establish the effects of vitamin supplements on mortality. The use of vitamin E reduced the risk of death from all causes by 34%. Effects were strongest for coronary artery disease, where vitamin E resulted in a 63% reduction in death from heart attack. In addition, use of vitamin E resulted in a 59% reduction in cancer mortality. When the effects of vitamins C and E were combined, overall mortality was reduced by 42% (compared to 34% for vitamin E alone) (Losonczy 1996). These results provided significant evidence about the value of vitamin supplementation, yet the media failed to report on it. It included 11 178 people, a larger group than most previous studies.

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