ASGSB 2003 Annual Meeting Abstracts


CLENBUTEROL'S NEUROPROTECTIVE EFFECT ON UV-C EXPOSED HUMAN RETINAL CELLS. A.W. von Deutsch1,2, D.A. von Deutsch2,3,4, I.K. Abukhalaf2,3,4, D. Ellerson5 , K. Dutt6, T.C. Chu3, and S. Houston21Collins Hill High School, Lawrenceville, GA.; 2Space Medicine and Life Sciences Research Center, 3Department of Pharmacology & Toxicology, and the 4Clinical Research Center, 5Department of Biochemistry, Immunology, and Microbiology, 6Department of Pathology, Morehouse School of Medicine, Atlanta, GA 30310.

   During spaceflight, astronauts are continuously exposed to low levels of radiation and experience varying degrees of ischemia and reperfusion-related oxidative damage. Furthermore, oxidative stress can also arise from ionizing and ultraviolet radiation (UV). The latter provides a relatively safe approach for studying the effects of radiation-induced free radical-mediated cellular damage. The purpose of this study was two fold. First, to establish the extent of UV-induced damaged in human retinal cells and second, to find whether damage could be attenuated by treatment with 10-7 M clenbuterol, a 2-adrenergic agonist. Methods. Human fetal retinal cells were cultured in 6-well trays with half of the wells receiving treatment and the other vehicle (PBS). Trays were exposed to UV-C for varying lengths of time (0, 15, 30, 60, and 90 minutes). At 24 hours post-exposure, the trays were pulled and cell vitality was checked by dye exclusion assay. Subsequent experiments used a fixed exposure time of 90 minutes to UV-C to determine the effects of the 2-adrenoceptor antagonist ICI-118551 (10-6 M) and the ornithine decarboxylase inhibitor difluoromethylornithine (DFMO, 10-5 M) on clenbuterol's protective effects. Results. Treatment with 10-7 M clenbuterol significantly reduced the rate of cell death due to UV-C exposure at all exposure times. Furthermore, the 2-adrenoceptor antagonist ICI-118551 significantly attenuated clenbuterol's protective effect while DFMO completely blocked it. Conclusions: This study suggests that the neuroprotective effect of clenbuterol is mediated through polyamines.

(This work was supported, in part, by NASA Grant NCC9-112 and NIH Grants RCRII 2P20, RR11104-09, and 5P20RR11104-7)


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