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- Title
We should protect our cells and telomeres from oxidative stress: A review of aging mechanisms.
- Authors
TÜRK, Bilge AYDIN
- Abstract
Aging (senescence) is a natural biological process that is the result of several different cellular senescence mechanisms causing a progressive functional cell capacity reduction. The most important mechanism is the free radical theory proposed by Denham Harman, also known as mitochondrial aging theory. Free oxygen radicals are extremely unstable substances with an unpaired electron in their outer orbital and their accumulation leads oxidative stress. Aging begins as the body's defense mechanisms against free radicals with a variety of enzymes and some antioxidants diminish over time. Another theory is the replicative aging theory described by Hayflick. Telomeres are specific DNA sequence repeats that make up the end of chromosomes. As a result of every cell division, telomeres become shorter and trigger aging-related mechanisms when it reaches a critical length. The telomere length is protected by addition of nucleotides which is mediated by an enzyme called telomerase, which is not present in the majority of somatic cells. Telomerase activity is regained in immortalized cancer cells, providing infinite multiplication capacity to cancer cells. Although these mechanisms seem to be independent, several studies have shown that oxidative stress is also effective in shortening of telomeres. The shortening rate of telomeres in each cell division varies, affected by the balance between oxidative stress and antioxidant defense. In conclusion, decompensated oxidative stress plays a major role in the pathogenesis of aging related diseases such as cardiovascular diseases, Alzheimer's, and cancer. A stress-reduced lifestyle with regular exercise, an antioxidant-rich diet and avoiding alcohol and smoking seem to be our best defense against oxidative stress and, therefore, aging related diseases.
- Publication
Journal of Cellular Neuroscience & Oxidative Stress, 2018, Vol 10, Issue 2, p711
- ISSN
2149-7222
- Publication type
Academic Journal