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1 Department of Medicine, Rhode Island Hospital and Brown University School of Medicine, Providence, RI, USA
* To whom correspondence should be addressed. E-mail: Jose_Behar{at}brown.edu.
H2O2 and TCDC impair the contraction induced by CCK-8, ACh and KCl without affecting the actions of PGE2 and damage functions of membrane proteins except for PGE2 receptors. The aim of this study was to examine whether this preserved PGE2 actions contribute to cytoprotective mechanisms against reactive oxygen species. Muscle cells from guinea pig GB were obtained by enzymatic digestion. Levels of lipid peroxidation and activities of SOD and catalase were determined by spectrophotometry. Pretreatment with PGE2 prevented the inhibition of H2O2 or TCDC on agonists (CCK-8, ACh, KCl) induced contraction, reduced the expected increase in lipid peroxidation and activities of catalase and SOD caused by H2O2 and TCDC. Incubation with CCK-8 for 60 min desensitized CCK-1 receptors up to 30 min whereas no receptor desensitization was observed after PGE2-pretreatment. Cholesterol-rich liposomes treatment enhanced the inhibition of H2O2 and TCDC on agonists induced contraction including that of PGE2. Pretreatment with PGE2 prior to H2O2 and TCDC did not block completely their inhibition on agonists induced contraction. Cholesterol-rich liposomes treatment impaired the expected increase in catalase activities in response to PGE2. We conclude that pretreatment with PGE2 prevents the muscle cell damage caused by H2O2 and TCDC due to the resistance of PGE2 receptors to agonist induced desensitization. The preservation of PGE2 receptors may be designed to conserve these cytoprotective functions that are however impaired by the presence of excess cholesterol in the plasma membrane.
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