Hello everyone!
In most papers I looked in, it is mentioned that one of the main reasons why cells keep low resting cytosolic Ca2+ levels is that if high, it will interfere with ATP, precipitating.
Calcium phosphate salts indeed are water-insoluble, however I could not find any experimental evidence (e.g., EPR, or similar) that could prove the above statement.
I found in mitochondria Ca2+ salts indeed can precipitate, under Ca2+ overload conditions. But the above argument does not look too solid knowing there is ATP in the ER lumen (e.g. Article ATP Increases within the Lumen of the Endoplasmic Reticulum ...
), characterized also by Ca2+ levels significantly higher than in the cytosol.Do you know about experiments that had shown Ca2+-ATP precipitation in the cytosol? Or is there some mechanism allowing the cell to handle the solubility of these types of compounds?
Thank you for any insight!
In the meantime, intracellular calcium levels were mostly investigated by measuring transmembrane fluxes of the radioisotope 45Ca. It is possible to measure changes in total cell [Ca2+] by this means, but impossible to determine how concentrations have changed within particular intracellular compartments, such as in the cytosol. A better alternative was provided by jelly fish from which the Ca2+-activated light-emitting protein aequorin can be extracted (Shimomura and Johnson, 1969). Its molecular mass is 22 kDa and it cannot cross membranes, so prior to the era of transfection techniques, its use was limited to larger cell types into which it could be microinjected. Once in the cytosol, an increase in free Ca2+concentration causes the protein to release a pulse of light. Intracellular calcium concentration increases shortly after the onset of hypoxia. Voltage-gated calcium channels open in response to the falling transmembrane potential, and the increasing intracellular sodium concentration causes the membrane-bound Na/Ca exchanger to reverse its activity. An altered transmembrane potential is detected within the cell by ryanodine receptors on intracellular organelles leading to release of calcium from the endoplasmic reticulum and mitochondria. This increase in intracellular calcium is generally harmful, causing the activation of ATPase enzymes just when ATP may be critically low, the activation of proteases to damage sarcolemma and the cytoskeleton and the uncontrolled release of neurotransmitters (see later). At this stage, the cell has probably not been irretrievably damaged by spontaneous depolarization, but derangement of calcium channel function effectively prevents normal synaptic transmission and therefore cellular function. Extracellular adenosine, formed from the degradation of AMP, is also believed to play a role in blocking calcium channels during anoxia.
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