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XXII. BIOCHEMICKÝ ZJAZD - Jesseniova lekárska fakulta

XXII. BIOCHEMICKÝ ZJAZD - Jesseniova lekárska fakulta

XXII. BIOCHEMICKÝ ZJAZD - Jesseniova lekárska fakulta

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Lectures<br />

EffECT of aDENINE NUCLEOTIDES aND Mg 2+ IONS ON<br />

MITOCHONDrial CHLOrIDE CHaNNELS<br />

Viera Kominková, Zuzana Tomášková, Ľubica Máleková and Karol Ondriaš<br />

Institute of molecular physiology and genetics, Slovak Academy of Sciences,<br />

Bratislava, Slovak Republic<br />

Chloride channels are involved in many physiological and pathological processes such<br />

as the apoptosis, stress, reperfusion injury or cardioprotection. The cells in ischemic<br />

tissues are depleted of oxygen and lose their capacity for ATP production. Due to this<br />

energy deprivation, destructive processes are activated which lead to cell injury or death.<br />

Molecular mechanisms of these processes are still not fully understood. The aim of our<br />

work was to study the possible role of mitochondrial chloride channels in these processes.<br />

We report the effect of adenine nucleotides (ATP, ADP and AMP-PNP) and Mg 2+ on the<br />

activity of mitochondrial chloride channels. Submitochondrial vesicles isolated from<br />

rat heart were incorporated into bilayer lipid membrane and single chloride channel<br />

currents were measured. We found that ATP inhibited chloride channels and affected<br />

both kinetics and current amplitude. This inhibitory effect was not dependent on phosphorylation<br />

of the channel. Furthermore, ADP did not affect the channel activity but<br />

only decreased the current amplitude. When the effect of ATP was studied in Mg 2+ free<br />

solutions, a hyperbolic current-voltage relationship was observed after addition of ATP.<br />

Addition of MgCl 2<br />

(up to 5mmol/L) partially relieved this effect of ATP.<br />

ATP, within the range of physiological concentrations, inhibits the mitochondrial chloride<br />

channels, which invokes a hypothesis that these channels have a role during pathological<br />

processes connected with ATP depletion.<br />

Acknowledgements: This work was supported by VEGA 2/0150/10 and VVCE-0064-07.<br />

<strong>XXII</strong>. Biochemistry Congress, Martin<br />

103

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