Involvement of intracellular chloride and promiscuous channels in apoptosis and cardioprotection

ONDRIAŠ, Karol, Lubica MALEKOVÁ, Vladimíra KOMÍNKOVÁ, Juraj KOPÁČEK, Olga KRIŽANOVÁ a Marie NOVÁKOVÁ. Involvement of intracellular chloride and promiscuous channels in apoptosis and cardioprotection. Acta Physiologica. Oxford: Blackwell Publishing, 2007, roč. 191, Suppl 658, s. 70-70. ISSN 1748-1708.

Základní údaje

Originální název

Involvement of intracellular chloride and promiscuous channels in apoptosis and cardioprotection

Název česky

Úloha nitrobuněčných chloridových a nespecifických kanálů v apoptóze a kardioprotekci

Autoři

ONDRIAŠ, Karol, Lubica MALEKOVÁ, Vladimíra KOMÍNKOVÁ, Juraj KOPÁČEK, Olga KRIŽANOVÁ a Marie NOVÁKOVÁ

Vydání

Acta Physiologica, Oxford, Blackwell Publishing, 2007, 1748-1708

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Další údaje

Jazyk

angličtina

Typ výsledku

Článek v odborném periodiku

Obor

30105 Physiology

Stát vydavatele

Velká Británie a Severní Irsko

Utajení

není předmětem státního či obchodního tajemství

Impakt faktor

Impact factor: 1.602

Organizační jednotka

Lékařská fakulta

Klíčová slova anglicky

chloride channels;mitochondrial promiscuos channels;apoptosis;cardioprotection

Štítky

apoptosis, cardioprotection, chloride channels, mitochondrial promiscuos channels

Příznaky

Mezinárodní význam, Recenzováno

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Anotace

V originále

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.

Česky

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.