Oxidative Stress Causes Aging: Genetics and Epigenetics

Merit Research Journals
Publication Type:
Journal Article
Merit Research Journal of Medicine and Medical Sciences, 2017, 5 (12), pp. 604 - 610 (6)
Issue Date:
Full metadata record
Files in This Item:
Filename Description Size
Shahbaz (9).pdfPublished Version387.37 kB
Adobe PDF
Reactive Oxygen Species (ROS) if increase abnormally cause oxidative stress (OS) resulting in aging ultimately involve genetic and epigenetic factors. Oxidative stress (OS) depicts a disparity among the systemic manifestation of reactive oxygen species and a living system’s ability to knowingly detoxify the reactive intermediates or otherwise to repair the ultimate loss. Turbulence in the normal redox state of the cells may cause toxic effects through the production of peroxides and free radicals that damage all gears of the cell, mainly DNA, proteins and lipids. Oxidative stress (OS) in aging brain has shown remarkable damage with memory decays causing Alzheimer’s disease. Oxidative stress (OS) occurs when any of the molecules in the body get in touch with reactive oxygen species. These molecules become oxidized or “burned” and lose an electron and become excited. They wander around and cause damage to cells at organelle (mitochondria ‘mt’ and endoplasmic reticulum ‘ER’) and genetic level (transcriptional changes, genome instability), if they aren’t “cleaned up” neutralized or balanced. The effect is accelerated aging, finally leading to death. Progeria is accelerated aging due to a genetic disorder. If we posit the agents responsible for oxidative stress, for example, glutathione; aging may be delayed. Present study will strongly focus to revolutionize the management plan for oxidative stress (OS) and longevity. This review emphasizes on oxidative stress, reasons for oxidative stress, what ROS does with genes and main impact of those effects on aging.
Please use this identifier to cite or link to this item: