Role of superoxide dismutase enzymes and ascorbate in protection of nitrergic relaxation against superoxide anions in mouse duodenum
Autor: | Nuran Ogulener, Olcay Ergurhan Kiroǧlu, M. Ata Seçilmiş |
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Přispěvatelé: | Çukurova Üniversitesi |
Jazyk: | angličtina |
Rok vydání: | 2008 |
Předmět: |
Male
Duodenum Muscle Relaxation Ascorbic Acid In Vitro Techniques Nitric Oxide digestive system Antioxidants Superoxide dismutase chemistry.chemical_compound Mice Manganese superoxide dismutase Superoxides Organometallic Compounds Animals Pharmacology (medical) Pharmacology chemistry.chemical_classification biology Estradiol Superoxide Superoxide Dismutase digestive oral and skin physiology Superoxide anion generators Muscle Smooth General Medicine Free Radical Scavengers Mouse Duodenum Ethylenediamines Oxidants Manganese Superoxide Dismutase Endogenous superoxide dismutase Enzyme Biochemistry chemistry biology.protein Female Mouse duodenum |
Popis: | PubMedID: 18501115 Aim: The aim of this study was to investigate whether superoxide dismutase (SOD) enzymes and ascorbate play a role in the protection of the nitrergic relaxation against superoxide anion inhibition in the mouse duodenum. Methods: The effects of exogenous SOD, N,N'-bis(salicylidene) ethylenediamine chloride (EUK-8; a synthetic cell-permeable mimetic of the manganese SOD [Mn SOD] and ascorbate on relaxant responses induced by nitrergic nerve stimulation), exogenous nitric oxide (NO), and nitroglycerin were investigated in isolated mouse duodenum tissues. Results: Diethyldithiocarbamate (DETCA) inhibited the relaxation to exogenous NO and nitroglycerin, but not relaxation to electrical field stimulation (EFS). SOD and ascorbate partially prevented the inhibitory effect of DETCA on relaxation to NO, abut not to nitroglycerin. The DETCA-induced inhibition on nitroglycerin was prevented by EUK-8. Hemoglobin, 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazolinel-oxyl-3-oxide, and hydroxo-cobalamin inhibited the relaxation to NO, but not to EFS and nitroglycerin in the presence of DETCA. Pyrogallol and hydroquinone inhibited the relaxation to NO, but not to EFS and nitroglycerin. This inhibition was prevented by exogenous SOD and ascorbate, but was not prevented by EUK-8. Pyrogallol and hy-droquinone did not inhibit the EFS-induced relaxation in the presence of DETCA. Duroquinone and 6-anilino-5.8-quinolinedione inhibited the relaxation to EFS, NO, and nitroglycerin, and this inhibition was prevented by EUK-8. Conclusion: These results suggest that the nitrergic neurotransmission in the mouse duodenum is protected by endogenous tissue antioxidants against superoxide anions, and Mn SOD, in addition to copper/zinc SOD, can protect NO from attack from superoxide anion generators intracellularly. Also, the possibility that the endogenous neurotransmitter may not be the free NO but a NO-containing or NO-generating molecule in the mouse duodenum remains open. © 2008 CPS and SIMM. |
Databáze: | OpenAIRE |
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