Effect of Arachidonic Acid on Conductive Na, K and Anion Transport in Ehrlich Ascites Tumor Cells under Isotonic and Hypotonic Conditions

1991 ◽  
Vol 1 (4) ◽  
pp. 177-194 ◽  
Author(s):  
Ian Henry Lambert
Keyword(s):  
Arachidonic Acid ◽  
Tumor Cells ◽  
Anion Transport ◽  
Ehrlich Ascites Tumor ◽  
Ehrlich Ascites Tumor Cells ◽  
Ascites Tumor ◽  
Ehrlich Ascites

Dietary n-3 and n-6 fatty acids are equipotent in stimulating volume regulation in Ehrlich ascites tumor cells

1993 ◽  
Vol 264 (1) ◽  
pp. C109-C117 ◽  
Author(s):  
L. Lauritzen ◽  
E. K. Hoffmann ◽  
H. S. Hansen ◽  
B. Jensen
Keyword(s):  
Fatty Acids ◽  
Arachidonic Acid ◽  
Eicosapentaenoic Acid ◽  
Fish Oil ◽  
Tumor Cells ◽  
Initial Rate ◽  
Ehrlich Ascites Tumor ◽  
Ehrlich Ascites Tumor Cells ◽  
Ascites Tumor ◽  
Ehrlich Ascites

This investigation addresses whether enriching cellular phospholipids with n-3 or n-6 fatty acids affects the process of regulatory volume decrease (RVD) in murine Ehrlich ascites tumor cells. Two weeks of dietary n-3-rich fish oil (7.5%, wt/wt) increased the ratio of eicosapentaenoic acid to arachidonic acid in cellular phospholipids compared with an olive oil control diet. Cells grown in mice fed on fish oil had an accelerated RVD response after hypotonic exposure, indicating that the volume-induced K+ conductance was increased. The fish oil diet furthermore resulted in an increased Cl- conductance during RVD, demonstrated as an increased initial rate of cell shrinkage after addition of K+ ionophore to the swollen cells. The initial rate of volume recovery correlated positively with the sum of eicosanoid precursors (arachidonic acid plus eicosapentaenoic acid) (P = 0.007). Diet supplemented with n-6 fatty acids resulted in an enhanced RVD response as well. RVD was inhibited by anti-calmodulin drugs, and exogenous leukotriene D5 and leukotriene D4 were equipotent in attenuating this inhibition. We conclude that dietary polyunsaturated fatty acids result in a more effective RVD response because of an increase in the volume-induced Cl- and K+ conductances. We propose that this is caused by an enhanced volume-induced leukotriene synthesis due to an increase in eicosanoid precursor availability.

Thrombin-, bradykinin-, and arachidonic acid-induced Ca2+ signaling in Ehrlich ascites tumor cells

1999 ◽  
Vol 276 (1) ◽  
pp. C26-C37 ◽  
Author(s):  
Nanna Koschmieder Jørgensen ◽  
Stine Falsig Petersen ◽  
Else Kay Hoffmann
Keyword(s):  
Arachidonic Acid ◽  
Tumor Cells ◽  
Structural Analog ◽  
Ehrlich Ascites Tumor ◽  
Induced Response ◽  
Ehrlich Ascites Tumor Cells ◽  
Ascites Tumor ◽  
Free Medium ◽  
Ehrlich Ascites ◽  
Intracellular Ca

Stimulation of single Ehrlich ascites tumor cells with agonists (bradykinin, thrombin) and with arachidonic acid (AA) induces increases in the free intracellular Ca2+ concentration ([Ca2+]i) in the presence and absence of extracellular Ca2+, measured using the Ca2+-sensitive probe fura 2. Sequential stimulation with two agonists elicits sequential increases in [Ca2+]i, unlike addition of the same agonist twice. Bradykinin and thrombin have additive effects on [Ca2+]iin Ca2+-free medium. The phosphoinositidase C inhibitor U-73122 inhibits the agonist-induced increases in [Ca2+]i, whereas ryanodine has no effect. Pretreatment of cells in Ca2+-free medium with thapsigargin abolishes the bradykinin-induced increase in [Ca2+]ibut not the response to thrombin. The AA-induced response is not inhibited by U-73122 and cannot be mimicked by the inactive structural analog trifluoromethylarachidonyl ketone. Pretreatment of the cells with 50 μM AA (but not with 10 μM AA) abolishes the agonist-induced increase in [Ca2+]i. Thus bradykinin, thrombin, and AA induce increases in [Ca2+]iin Ehrlich cells due to Ca2+ entry and release from intracellular stores. Thrombin causes release of Ca2+ from an intracellular store that is insensitive to bradykinin and is not depleted by thapsigargin but is depleted by AA.

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