Vasoconstriction and bronchoconstriction induced by 2,5-Di(tert-butyl)1,4-benzohydroquinone, an endoplasmic reticular Ca2+-ATPase inhibitor in isolated and perfused rat lung

1992 ◽  
Vol 36 (1-2) ◽  
pp. 33-38 ◽  
Author(s):  
L. Atzori ◽  
G. Bannenberg ◽  
A. M. Corriga ◽  
Å Ryrfeldt ◽  
P. Moldeus
Keyword(s):  
Rat Lung ◽  
Atpase Inhibitor ◽  
Tert Butyl

Evidence for two intracellular calcium pools in Dictyostelium: the cAMP-induced calcium influx is directed into a NBD-Cl- and 2,5-di-(tert-butyl)1,4-hydroquinone-sensitive pool

1993 ◽  
Vol 105 (4) ◽  
pp. 1131-1135 ◽  
Author(s):  
H. Flaadt ◽  
E. Jaworski ◽  
D. Malchow
Keyword(s):  
Calcium Influx ◽  
Fine Tuning ◽  
Cell Surface Receptor ◽  
Bafilomycin A1 ◽  
Atpase Inhibitor ◽  
Tert Butyl ◽  
Cellular Events ◽  
Surface Receptor ◽  
Oriented Movement ◽  
Gamma S

Signal transduction in Dictyostelium for oriented movement and differentiation involves a fine tuning of the cytosolic Ca2+ concentration. We have previously shown that cAMP binding to the cell surface receptor elicits two cellular events: (i) to enhance Ca2+ entry across the plasma membrane; (ii) to increase Ca2+ uptake into Ca(2+)-sequestering organelles. Here we used permeabilised cells to show that cAMP-induced Ca2+ uptake in these cells was sensitive to the Ca2+ transport ATPase blocker 2,5-di-(tert-butyl)-1,4-hydroquinone (BHQ) and the vacuolar H(+)-ATPase inhibitor NBD-Cl. By contrast, bafilomycin A1 and vanadate, inhibitors of Ca2+ uptake into acidosomes in Dictyostelium, did not reduce the cAMP-induced Ca2+ uptake of permeabilised cells. GTP gamma S served as a tool to measure Ins(1,4,5)P3- (InsP3)-sensitive Ca2+ release. Following NBD-Cl or BHQ treatment Ca2+ release was reversibly inhibited. We conclude that the cAMP-controlled Ca2+ influx is directed into a NBD-Cl and BHQ-sensitive compartment, which comprises the InsP3-releasable pool. The acidosomal Ca2+ store seems to provide for additional Ca2+ if required.

Response of human spermatozoa to an internal calcium ATPase inhibitor, 2,5-di(tert-butyl) hydroquinone

1997 ◽  
Vol 279 (3) ◽  
pp. 284-290 ◽  
Author(s):  
Raquel L. Perry ◽  
Christopher L. R. Barratt ◽  
Michael A. Warren ◽  
Ian D. Cooke
Keyword(s):  
Calcium Atpase ◽  
Human Spermatozoa ◽  
Atpase Inhibitor ◽  
Tert Butyl ◽  
Internal Calcium

scholarly journals Two classes of agonist-sensitive Ca2+ stores in platelets, as identified by their differential sensitivity to 2,5-di-(tert-butyl)-1,4-benzohydroquinone and thapsigargin

1995 ◽  
Vol 310 (2) ◽  
pp. 449-452 ◽  
Author(s):  
L Cavallini ◽  
M Coassin ◽  
A Alexandre
Keyword(s):  
The Other ◽  
Differential Sensitivity ◽  
Atpase Inhibitor ◽  
Substantial Fraction ◽  
Tert Butyl ◽  
Store Depletion ◽  
Different Types ◽  
Combined Action

In the absence of extracellular Ca2+, extensive Ca2+ release from the platelet intracellular stores [monitored as an increase of intracellular Ca2+ concentration ([Ca2+]i)] is produced by the combined action of the endomembrane Ca(2+)-ATPase inhibitor thapsigargin and 2 nM ionomycin. The titration of Ca2+ unloading with thapsigargin (plus ionomycin) shows that a substantial fraction of the store-associated Ca2+ is released by 8-10 nM thapsigargin, but that 100-200 nM thapsigargin is required for the complete release. The store depletion obtained in similar conditions with a different endomembrane Ca(2+)-ATPase inhibitor, 2,5-di-(tert-butyl)-1,4-benzohydroquinone (TBHQ), is always incomplete. It is completed by thrombin or by 10 nM thapsigargin. We conclude that two different types of Ca2+ pumps exist in platelets, one sensitive to TBHQ and to high thapsigargin, the other insensitive to TBHQ and sensitive to low thapsigargin. They are distributed separately in discrete subpopulations of the agonist-sensitive stores. The influx of external Ca2+ is maximal when both types of stores are Ca(2+)-depleted, either by high thapsigargin or by the combined action of low thapsigargin and TBHQ.

Rat lung glutathione release: response to oxidative stress and selenium deficiency

1987 ◽  
Vol 62 (1) ◽  
pp. 55-60 ◽  
Author(s):  
S. G. Jenkinson ◽  
T. H. Spence ◽  
R. A. Lawrence ◽  
K. E. Hill ◽  
C. A. Duncan ◽  
...  
Keyword(s):  
Reductase Activity ◽  
Selenium Deficiency ◽  
Rat Lung ◽  
Free Radical Damage ◽  
Butyl Hydroperoxide ◽  
Tert Butyl ◽  
Rat Lungs ◽  
Tert Butyl Hydroperoxide ◽  
Glutathione Reductase Activity ◽  
Proportional Increase

We performed experiments to characterize the glutathione-dependent metabolism occurring during tert-butyl hydroperoxide infusion in isolated perfused rat lungs and to examine the effect of selenium deficiency on this metabolism. Selenium deficiency resulted in decreased lung glutathione peroxidase activity but normal glutathione reductase activity and glutathione content. Infusion of the hydroperoxide into control lungs caused a proportional increase in tissue glutathione disulfide (GSSG) concentration and release of GSSG into the perfusate up to an infusion rate of 250 nmol of tert-butyl hydroperoxide X min-1 X 100 g body wt-1. Infusion rates greater than this resulted in continued rise of tissue GSSG concentrations but GSSG release into the perfusate plateaued. Infusion of tert-butyl hydroperoxide into selenium-deficient rat lungs resulted in much lower concentrations of tissue GSSG and GSSG release into the perfusate; however, release in the selenium-deficient rat lung was also found to be saturable at infusion rates of 450 nmol of tert-butyl hydroperoxide X min-1 X 100 g of body wt-1. Selenium deficiency in the rat decreases the rate of reduction of infused tert-butyl hydroperoxide by glutathione and may predispose the lung to free radical damage.

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