Ukr.Biochem.J. 2012; Volume 84, Issue 5, Sep-Oct, pp. 76-88

Endoplasmic-mitochonrial Са(2+)-functional unit: dependence of respiration of secretory cells on activity of ryanodine- and IP(3)-sensitive Ca(2+)-channels

O. Yu. Velykopolska, B. O. Manko, V. V. Manko

Ivan Franko National University of Lviv, Ukraine;

Using Clark oxygen electrode, dependence of mitochondrial functions on Ca2+-release channels activity of Chironomus plumosus L. larvae salivary glands suspension was investigated. Cells were ATP-permeabilized in order to enable penetration of exogenous oxidative substrates. Activation of plasmalemmal P2X-receptors (as well as P2Y- receptors) per se does not modify the endogenous respiration of salivary gland suspension. That is, Ca2+-influx from extracellular medium does not influence functional activity of mitochondria, although they are located along the basal part of the plasma membrane. Activation of RyRs intensifies endogenous respiration and pyruvate-malate-stimulated respiration, but not succinate-stimulated respiration. Neither activation of IP3Rs (via P2Y-receptors activation), nor their inhibition alters endogenous respiration. Nevertheless, IP3Rs inhibition by 2-APB intensifies succinate-stimulated respiration. All abovementioned facts testify that Са2+, released from stores via channels, alters functional activity of mitochondria, and undoubted­ly confirm the existence of endoplasmic-mitochondrial Ca2+-functional unit in Ch. plumosus larvae salivary glands secretory cells. In steady state of endoplasmic-mitochondrial Ca2+-functional unit the spontaneous activity of IP3Rs is observed; released through IP3Rs, Ca2+ is accumulated in mitochondria via uniporter and modulates oxidative processes. Activation of RyRs induces the transition of endoplasmic-mitochondrial Ca2+-functional unit to the active state, which is required to intensify cell respiration and oxidative phosphorylation. As expected, the transition of endoplasmic-mitochondrial Ca2+-functional unit to inactivated state (i. e. inhibition of Ca2+-release channels at excessive [Ca2+]i) limits the duration of signal transduction, has protective nature and prevents apoptosis.

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