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S.G. Jarrett, M.E. Boulton; RPE Cells Demonstrate Greater Resistance Towards Oxidative Stress Compared to Other Cell Types . Invest. Ophthalmol. Vis. Sci. 2003;44(13):1641.
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Purpose: To test the hypothesis that the local environment (high oxygenation and visible light) has resulted in retinal pigment epithelium (RPE) cells developing a greater resistance to oxidative stress compared to other human cell types. Methods: The cytotoxity of various oxidative stressors (tert-butylhydroperoxide (t-BOOH), hydrogen peroxide (H202), Paraquat (PA), and sodium arsenite (NaA2)) upon human primary retinal pigment epithelial cells (hRPE), a RPE cell line (ARPE-19), human primary corneal fibroblasts, human primary scleral fibroblasts, a liver hepatocyte cell line (HEP3B), a skin epidermal cell line (A431) and a aveolar type II cell line (A549) was determined as a measure of their respective LD50 values. Cell viability was assessed via the mitochondrial reduction of 3-(4,5-dimethylthiazol-2yl)-2,5-diphenyl tetrazolium bromide (MTT). Results: The seven different cell types demonstrated significantly different capacities in preventing cell death initiated by oxidative injury. However, for all oxidative stress inducing agents both hRPE and ARPE-19 possessed a significantly greater resistance, in comparison to all the other cell types. A greater resistance towards t-BOOH occurred up to 12hr after initial exposure (p<0.001); towards H202 up to 3hr (p<0.001); towards PA up to 48hr (p<0.01) and towards NaA2 up to 24hr (p<0.01). Furthermore, a significant difference in the cytotoxic potency of the four oxidative inducers was observed. The extent of cellular damage was consistent with the generation of various reactive oxygen species (ROS) with varying magnitudes of cellular toxicity. The order of toxicity of the oxidative stress inducing compounds towards all the cell types was ranked H202> t-BOOH> NaA2> PA. Conclusions: The greater resistance of RPE cells to a diverse range of ROS demonstrates a functional significance for cell survival. These findings suggest that this apparent increased intrinsic cellular protection may be attributed to a typical in vivo environment which involves exposure to high levels of oxidative stress.
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