ONDRIAŠ, Karol, Lubica MALEKOVÁ, Vladimíra KOMÍNKOVÁ, Juraj KOPÁČEK, Olga KRIŽANOVÁ and Marie NOVÁKOVÁ. Involvement of intracellular chloride and promiscuous channels in apoptosis and cardioprotection. Acta Physiologica. Oxford: Blackwell Publishing, vol. 191, Suppl 658, p. 70-70. ISSN 1748-1708. 2007.
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Basic information
Original name Involvement of intracellular chloride and promiscuous channels in apoptosis and cardioprotection
Name in Czech Úloha nitrobuněčných chloridových a nespecifických kanálů v apoptóze a kardioprotekci
Authors ONDRIAŠ, Karol, Lubica MALEKOVÁ, Vladimíra KOMÍNKOVÁ, Juraj KOPÁČEK, Olga KRIŽANOVÁ and Marie NOVÁKOVÁ.
Edition Acta Physiologica, Oxford, Blackwell Publishing, 2007, 1748-1708.
Other information
Original language English
Type of outcome Article in a journal
Field of Study 30105 Physiology
Country of publisher United Kingdom of Great Britain and Northern Ireland
Confidentiality degree is not subject to a state or trade secret
Impact factor Impact factor: 1.602
Organization unit Faculty of Medicine
Keywords in English chloride channels;mitochondrial promiscuos channels;apoptosis;cardioprotection
Tags apoptosis, cardioprotection, chloride channels, mitochondrial promiscuos channels
Tags International impact, Reviewed
Changed by Changed by: prof. MUDr. Marie Nováková, Ph.D., učo 1188. Changed: 19/6/2009 15:54.
Abstract
Aims: Purpose of the study was to test the hypothesis that intracellular chloride and mitochondrial promiscuous channels are involved in the apoptosis and cardioprotection. Methods: We measured effects of the chloride blockers DIDS, NPPB and Phloretin on H2O2-induced cardiomyocyte apoptosis and single channel properties of chloride and high conductance promiscuous channels derived from rat heart lysosomal and mitochondrial membranes incorporated in bilayer lipid membrane (BLM). Promiscuity of the single mitochondrial channels was measured as a voltage change of a voltage-dependent switch from K+ to Cl- selectivity and an opposite switch. Results: The chloride channel blockers (100 micromol/l) inhibited the H2O2 induced cardiomyocytes apoptosis. They inhibited the chloride channels at concentrations of 10-50 micromol/l by decreasing the channel open probability and the open dwell time. They affected promiscuity of the mitochondrial high conductance channels, influencing the voltage-switch and the K+/Cl- channel activity. Conclusion: The obtained results did not contradict the tested hypothesis. We may assume that the intracellular and the promiscuous channels may be involved in apoptosis and cardioprotection, however a definite proof is still missing. The results may contribute to understand a possible involvement of intracellular chloride and promiscuous channels in apoptosis and cardioprotection.
Abstract (in Czech)
Aims: Purpose of the study was to test the hypothesis that intracellular chloride and mitochondrial promiscuous channels are involved in the apoptosis and cardioprotection. Methods: We measured effects of the chloride blockers DIDS, NPPB and Phloretin on H2O2-induced cardiomyocyte apoptosis and single channel properties of chloride and high conductance promiscuous channels derived from rat heart lysosomal and mitochondrial membranes incorporated in bilayer lipid membrane (BLM). Promiscuity of the single mitochondrial channels was measured as a voltage change of a voltage-dependent switch from K+ to Cl- selectivity and an opposite switch. Results: The chloride channel blockers (100 micromol/l) inhibited the H2O2 induced cardiomyocytes apoptosis. They inhibited the chloride channels at concentrations of 10-50 micromol/l by decreasing the channel open probability and the open dwell time. They affected promiscuity of the mitochondrial high conductance channels, influencing the voltage-switch and the K+/Cl- channel activity. Conclusion: The obtained results did not contradict the tested hypothesis. We may assume that the intracellular and the promiscuous channels may be involved in apoptosis and cardioprotection, however a definite proof is still missing. The results may contribute to understand a possible involvement of intracellular chloride and promiscuous channels in apoptosis and cardioprotection.
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