Cellular damage in the rat heart caused by caffeine or dinitrophenol |
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| Affiliation: | 1. Faculty of Science, Department of Biochemistry, University of Dschang, Dschang, Cameroon;2. Department of Pharmaceutical Biology, Institute of Pharmacy and Biochemistry, University of Mainz, Mainz, Germany;1. Department of Ocean Sciences, University of California, Santa Cruz, 1156 High Street, Santa Cruz, CA 95064, USA;2. Institute of Marine Sciences, University of California, Santa Cruz, 1156 High St., Santa Cruz, CA 95064, USA;3. Department of Earth and Planetary Sciences, University of California, Santa Cruz, 1156 High Street, Santa Cruz, CA 95064, USA;4. Environmental Studies, University of California, Santa Cruz, 1156 High St., Santa Cruz, CA 95064, USA;5. Department of Ecology and Evolutionary Biology, University of California, Santa Cruz, 1156 High Street, Santa Cruz, CA 95064, USA;1. Dipartimento di Chimica Industriale ‘Toso Montanari’, Università di Bologna, Viale Risorgimento 4, 40136 Bologna, Italy;2. Dipartimento di Fisica e Astronomia, Università di Bologna, Viale Berti Pichat 6/2, 40127 Bologna, Italy;3. Centro Interdipartimentale per la Ricerca Industriale – Meccanica avanzata e materiali, Università di Bologna, Viale del Risorgimento 2, 40136, Bologna, Italy;1. Institute of Plasma Physics Chinese Academy of Sciences, Hefei, 230031, China;2. University of Science and Technology of China, Hefei, 230022, China;3. Lappeenranta University of Technology, Lappeenranta, 53810, Finland;4. Anhui Province Key Laboratory of Special Welding Technology, Huainan, 232000, China;1. National Reference Laboratory of Veterinary Drug Residues (HZAU) and MAO Key Laboratory for Detection of Veterinary Drug Residues, Huazhong Agricultural University, Wuhan, Hubei 430070, China;2. Department of Pharmacology and Toxicology, Faculty of Veterinary Medicine, Universidad Complutense de Madrid (UCM), and Research Institute Hospital 12 de Octubre (i+12), 28040 Madrid, Spain;3. MAO Laboratory for Risk Assessment of Quality and Safety of Livestock and Poultry Products, Huazhong Agricultural University, Wuhan, Hubei 430070, China;4. Hubei Collaborative Innovation Center for Animal Nutrition and Feed Safety, Wuhan, Hubei, China;1. Institute of Chemistry, Health and Food Sciences, The Faculty of Mathematics and Natural Sciences, Jan Długosz University in Częstochowa, Armii Krajowej 13/15, Częstochowa, 42-201, Poland;2. Division of Organic Chemistry, Centre of Molecular and Macromolecular Studies, Polish Academy of Sciences, Sienkiewicza 112, Łódź, 90-363, Poland |
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| Abstract: | 1. Langendorff-perfusion of rat hearts with either 10 mM caffeine or 1 mM 2,4-dinitrophenol (DNP) caused severe ultrastructural damage to the myofilaments and mitochondria that was similar to that found in a standard Ca2+-paradox.2. This damage occurred in the presence and absence of extracellular Ca2+3. Creatine kinase (CK) release (indicative of sarcolemma breakdown) was not recorded unless the caffeine- or DNP-perfusion was preceded by Ca2+0-depletion.4. It is concluded that: (i) the pathways leading to damage to the myofilaments and sarcolemma are independent; (ii) the CK release mechanism requires dual activation of Ca2+0-depletion plus a rise in [Ca2+]i; and (iii) current theories concerning the mechanisms underlying the genesis of the Ca2+-paradox are incorrect or incomplete. |
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