MALEKOVÁ, Lubica, Jana TOMÁŠKOVÁ, Marie NOVÁKOVÁ, Peter ŠTEFÁNIK, Juraj KOPÁČEK, Boris LAKATOŠ, Silvia PASTOREKOVÁ, Olga KRIŽANOVÁ, Albert BREIER and Karol ONDRIAŠ. Inhibitory effect of DIDS, NPPB, and phloretin on intracellular chloride channels. Pflügers Archiv - Eur.J. Physiol. Ulm: Springer, 2007, vol. 455, No 2, p. 349–357. ISSN 0031-6768.
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Basic information
Original name Inhibitory effect of DIDS, NPPB, and phloretin on intracellular chloride channels
Name in Czech Inhibiční účinek DIDS, NPPB a phloretinu na nitrobuněčné chloridové kanály
Authors MALEKOVÁ, Lubica (703 Slovakia), Jana TOMÁŠKOVÁ (703 Slovakia), Marie NOVÁKOVÁ (203 Czech Republic, guarantor), Peter ŠTEFÁNIK (703 Slovakia), Juraj KOPÁČEK (703 Slovakia), Boris LAKATOŠ (703 Slovakia), Silvia PASTOREKOVÁ (703 Slovakia), Olga KRIŽANOVÁ (703 Slovakia), Albert BREIER (703 Slovakia) and Karol ONDRIAŠ (703 Slovakia).
Edition Pflügers Archiv - Eur.J. Physiol. Ulm, Springer, 2007, 0031-6768.
Other information
Original language English
Type of outcome Article in a journal
Field of Study 30105 Physiology
Country of publisher Germany
Confidentiality degree is not subject to a state or trade secret
Impact factor Impact factor: 3.842
RIV identification code RIV/00216224:14110/07:00032705
Organization unit Faculty of Medicine
UT WoS 000249972600014
Keywords in English Mitochondria;cardiac myocytes;chloride channels;chloride conductance;apoptosis;single channel
Tags apoptosis, cardiac myocytes, chloride channels, chloride conductance, mitochondria, single channel
Tags International impact, Reviewed
Changed by Changed by: prof. MUDr. Marie Nováková, Ph.D., učo 1188. Changed: 2/4/2010 10:45.
Abstract
We studied the effects of the chloride channel blockers, 5-nitro-2-(phenylpropylamino)-benzoate (NPPB), dihydro-4,4 diisothiocyanostilbene-2,2-disulphonic acid (DIDS), and phloretin on H2O2-induced primary culture cardiomyocyte apoptosis and activity of intracellular chloride channels obtained from rat heart mitochondrial and lysosomal vesicles. The chloride channel blockers (100 micromol/l) inhibited the H2O2-induced cardiomyocytes apoptosis. We characterized the effect of the blockers on single channel properties of the chloride channels derived from the mitochondrial and lysosomal vesicles incorporated into a bilayer lipid membrane. The single chloride channel currents were measured in 250:50 mmol/l KCl cis/trans solutions. NPPB, DIDS, and phloretin inhibited the chloride channels by decreasing the channel open probability in a concentration-dependent manner with EC50 values of 42, 7, and 20 micromol/l, respectively. NPPB and phloretin inhibited the channels conductance and open dwell time, indicating that they could affect the chloride selective filter, pore permeability, and gating mechanism of the chloride channels. DIDS and NPPB inhibited the channels from the other side than bongkrekic acid and carboxyatractyloside. The results may contribute to understand a possible involvement of intracellular chloride channels in apoptosis and cardioprotection.
Abstract (in Czech)
Studovali jsme účinky blokátorů chloridových kanálů, 5-nitro-2-(phenylpropylamino)-benzoatu (NPPB), dihydro-4,4 diisothiocyanostilbene-2,2-disulphonic kyseliny(DIDS), and phloretinu na H2O2-indukovanou apoptozu v primární kultuře kardiomyocytů a na aktivitu intracelulárních chloridových kanálů získaných z mitochondriálních a lysosomálních veziklů kardiomyocytů potkana. Blokátory chloridových kanálů (100 micromol/l) inhibovaly H2O2-indukovanou apoptozu kardiomyocytů. Studovali jsme účinek blokátorů na vlastnosti jednotlivého chloridového z kanálu na tomto modelu. Proudy přes jednotlivý kanál byly měřeny v 250:50 mmol/l KCl cis/trans roztocích. NPPB, DIDS, and phloretin inhibovaly chloridové kanály snížením pravděpodobnosti otevření kanálu koncentračně závisle s hodnotou EC50 42, 7, and 20 micromol/l. NPPB a phloretin inhibovaly vedení kanálem. Mohly by zřejmě chloridový selektivní filtr, permeabilitu poru a vrátkovací mechanismus. Naše data by mohla přispět k porozumění možnému zapojení intracelulárních chloridových kanálů do apoptozy a kardioprotekce.
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