Inhibitory effect of DIDS, NPPB, and phloretin on intracellular chloride channels View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2007-07-05

AUTHORS

Lubica Malekova, Jana Tomaskova, Marie Novakova, Peter Stefanik, Juraj Kopacek, Boris Lakatos, Silvia Pastorekova, Olga Krizanova, Albert Breier, Karol Ondrias

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 μmol/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 μmol/l, respectively. NPPB and phloretin inhibited the channel’s 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. More... »

PAGES

349-357

References to SciGraph publications

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s00424-007-0300-9

DOI

http://dx.doi.org/10.1007/s00424-007-0300-9

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1020999212

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/17611769


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