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Oxidative stress induces senescence in cultured RPE cell

11.14.16 | Bentham Science Publishers

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Age-related macular degeneration (AMD) is a leading cause of worldwide blindness in the elderly. It is a bilateral ocular condition that impairs the central retina known as the macula. The macula accounts for the majority of daytime, color vision in humans. Thus, lesions in the macula have a major impact on human vision. Previous studies have suggested that oxidative stress to certain ocular cells may contribute to the development of AMD. Oxidative stress occurs when reactive oxygen species (ROS) interact with protein and DNA to modify their functions. In this study, Aryan et al used hydrogen peroxide, a highly reactive compound, to induce oxidative stress in human retinal pigment epithelial cells, a type of ocular cell which provides nourishment for the human retina. Oxidative stress resulted in a profound influence on advancing the senescence (functional deterioration) of these cells and inhibiting their proliferation. These results strongly suggest that oxidative stress plays a role in the development of AMD in our aging population. Additional studies on the role of antioxidants should provide a new treatment approach for the intervention of AMD in elderly patients.

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For more information about the article, please visit http://benthamopen.com/FULLTEXT/TONEUJ-10-83

DOI: 10.2174/1874205X01610010083

Reference: Aryan, N.; et al, (2016). Oxidative Stress Induces Senescence in Cultured RPE Cells, Open Neurol. J., DOI: 10.2174/1874205X01610010083

The Open Neurology Journal

10.2174/1874205X01610010083

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APA:
Bentham Science Publishers. (2016, November 14). Oxidative stress induces senescence in cultured RPE cell. Brightsurf News. https://www.brightsurf.com/news/LM26K4VL/oxidative-stress-induces-senescence-in-cultured-rpe-cell.html
MLA:
"Oxidative stress induces senescence in cultured RPE cell." Brightsurf News, Nov. 14 2016, https://www.brightsurf.com/news/LM26K4VL/oxidative-stress-induces-senescence-in-cultured-rpe-cell.html.