scholarly journals The role of cell calcium in current approaches to toxicology.

1990 ◽  
Vol 84 ◽  
pp. 7-15 ◽  
Author(s):  
J G Pounds
Keyword(s):  
2004 ◽  
Vol 22 (Suppl. 2) ◽  
pp. S187
Author(s):  
J. Loukotová ◽  
J. Tichá ◽  
J. Kunes ◽  
J. Zicha

1990 ◽  
Vol 258 (1) ◽  
pp. R222-R231
Author(s):  
J. A. Arruda ◽  
G. Dytko ◽  
Z. Talor

We studied the interaction of intracellular pH, exocytosis, and cell calcium on the stimulation of H+ secretion by CO2 in turtle bladder. Intracellular pH was continuously monitored by the fluorescent dye 6-carboxyfluorescein and exocytosis was monitored by the release of mucosal fluorescein dextran. The initial stimulation of H+ secretion by 1 or 5% CO2 added to the serosal solution was accompanied by a similar and temporally related increase in exocytosis. Furthermore, a decrease in intracellular pH seems necessary for the early increase in H+ secretion and exocytosis. Because calcium plays an important role in exocytosis, we measured intracellular calcium in isolated cells with the fluorescent dye quin2. An increase in intracellular calcium (from 50 to 100 nM) was observed in isolated turtle bladder epithelial cells gassed with 5% CO2. To further evaluate the role of intracellular calcium on H+ secretion and exocytosis we utilized agents that alter cell calcium such as trifluoperazine and lanthanum. In the presence of CO2 these agents blocked partially the increase in H+ secretion and exocytosis but did not affect the decrease in intracellular H+. In conclusion, exocytosis, intracellular pH, and intracellular calcium play a key role in mediating CO2-stimulated H+ secretion in the turtle bladder.


2008 ◽  
Vol 1777 ◽  
pp. S49
Author(s):  
Francesco M. Lasorsa ◽  
Paolo Pinton ◽  
Pasquale Scarcia ◽  
Luigi Palmieri ◽  
Rosario Rizzuto ◽  
...  

2019 ◽  
Vol 43 (4) ◽  
pp. 476-485
Author(s):  
Jack A. Rall

Lewis Victor Heilbrunn has been called the pioneer of Ca2+ as an intracellular regulator (Campbell AK. Cell Calcium 7: 287–296, 1986; Campbell AK. Intracellular Calcium, 2015). In 1947, he was the first to provide convincing evidence that Ca2+ triggered muscle contraction (Heilbrunn LV, Wiercinski FJ. J Cell Comp Physiol 29: 15–32, 1947). Yet his work was met mostly with silence and neglect. One wonders why. Heilbrunn was a general physiologist who believed in the uniformity of nature with regard to movement. He believed that “. . . the theory of what makes cells divide should not be very different from the theory of what makes muscle contract . . .” (Heilbrunn LV. The Dynamics of Living Protoplasm, 1956). He did not believe that one could understand how the living machine worked by investigating its parts. He believed that, to understand life, one must study the dynamics of living protoplasm. The origin and evolution of Heilbrunn’s thought process regarding the role of Ca2+ as a physiological activator will be traced back to the 1920s. The ways in which he tested the Ca2+ hypothesis in sea urchin eggs in the 1920s and 1930s will be explored. This work shaped Heilbrunn’s thinking about the role of Ca2+ in muscle contraction. Importantly, why he and his results were ignored for years will be examined. It turned out that being right was not enough. Bad luck and a stubborn belief in an outmoded scientific philosophy contributed to the neglect.


1993 ◽  
Vol 264 (5) ◽  
pp. C1165-C1170 ◽  
Author(s):  
S. M. Bagnasco ◽  
M. H. Montrose ◽  
J. S. Handler

Madin-Darby canine kidney (MDCK) cells accumulate the nonperturbing osmolytes myo-inositol and betaine when grown in hypertonic medium. When returned to isotonic conditions, there is a transient basolateral efflux of these osmolytes, contributing to regulatory volume decrease. Using fura-2 fluorescence, we estimated intracellular calcium concentrations after switching MDCK cells from 500 to 300 mosM medium. Cell calcium increased 565 +/- 93 nM within 5 min. Lowering extracellular calcium inhibited the increase in cell calcium and osmolyte efflux when cells were shifted from 500 to 300 mosM medium. The calcium channel blockers lanthanum and nifedipine also inhibited osmolyte efflux after the shift from 500 to 300 mosM. In the absence of change in medium tonicity, increasing cell calcium by exposure to 1 microM ionomycin did not alter osmolyte efflux. As in PAP-HT25 cells, the cytochrome P-450 inhibitors ketoconazole and SKF-525A inhibited the efflux of both osmolytes caused by a reduction in osmolarity. Thus an early rise in cell calcium that is dependent on extra-cellular calcium and a pathway blocked by inhibitors of cytochrome P-450 oxidase are critical in regulation of osmolyte efflux when MDCK cells are shifted from hypertonic to isotonic medium.


Cell Calcium ◽  
2005 ◽  
Vol 37 (6) ◽  
pp. 603
Author(s):  
L.S. Gray ◽  
E. Perez-Reyes ◽  
J.C. Gomora ◽  
D.M. Haverstick ◽  
M. Shattock ◽  
...  

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