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Title: The effect of mitochondrial inhibitors on calcium homeostasis in tumor mast cells

Abstract

The depletion of intracellular ATP by mitochondrial inhibitors in a glucose-free saline solution inhibited antigen-stimulated 45Ca uptake, the rise in cytoplasmic calcium, measured by fura-2, and secretion in rat basophilic leukemia cells. Lowering the intracellular ATP concentration also released calcium from an intracellular store and made further 45Ca efflux from the cells unresponsive to subsequent antigen stimulation. Antigen-stimulated 45Ca efflux could be restored by the addition of glucose. The ATP-sensitive calcium store appeared to be the same store that releases calcium in response to antigen. In contrast, intracellular ATP was not lowered, and antigen-stimulated secretion was unaffected by mitochondrial inhibitors, provided that glucose was present in the bathing solution. Similarly, antigen-stimulated 45Ca uptake, 45Ca efflux, and the rise in free ionized calcium were unaffected by individual mitochondrial inhibitors in the presence of glucose. However, when the respiratory chain inhibitor antimycin A was used in combination with the ATP synthetase inhibitor oligomycin in the presence of glucose, antigen-stimulated 45Ca uptake was inhibited, whereas the rise in free ionized calcium and secretion were unaffected. Also, antigen-induced depolarization (an indirect measurement of Ca2+ influx across the plasma membrane) was not affected. The inhibition of antigen-stimulated 45Ca uptake could, however, be overcome if amore » high concentration of the Ca2+ buffer quin2 was present in the cells to buffer the incoming 45Ca. These results suggest that in fully functional rat basophilic leukemia cells the majority of the calcium entering in response to antigen stimulation is initially buffered by a calcium store sensitive to antimycin A and oligomycin, presumably the mitochondria.« less

Authors:
;  [1]
  1. Cornell Univ., Ithaca (USA)
Publication Date:
OSTI Identifier:
6995015
Resource Type:
Journal Article
Journal Name:
American Journal of Physiology; (USA)
Additional Journal Information:
Journal Volume: 258; Journal ID: ISSN 0002-9513
Country of Publication:
United States
Language:
English
Subject:
59 BASIC BIOLOGICAL SCIENCES; ANTIGENS; BIOLOGICAL FUNCTIONS; CALCIUM; MEMBRANE TRANSPORT; ANTIMYCIN; ATP; CALCIUM 45; ENZYME INHIBITORS; FLUORESCENCE; GLUCOSE; HOMEOSTASIS; LEUKEMIA; MAST CELLS; MITOCHONDRIA; RATS; SURVIVAL TIME; TRACER TECHNIQUES; TUMOR CELLS; ALDEHYDES; ALKALINE EARTH ISOTOPES; ALKALINE EARTH METALS; ANIMAL CELLS; ANIMALS; ANTI-INFECTIVE AGENTS; ANTIBIOTICS; BETA DECAY RADIOISOTOPES; BETA-MINUS DECAY RADIOISOTOPES; CALCIUM ISOTOPES; CARBOHYDRATES; CELL CONSTITUENTS; CONNECTIVE TISSUE CELLS; DAYS LIVING RADIOISOTOPES; DISEASES; DRUGS; ELEMENTS; EVEN-ODD NUCLEI; FUNCTIONS; HEMIC DISEASES; HEXOSES; IMMUNE SYSTEM DISEASES; INTERMEDIATE MASS NUCLEI; ISOTOPE APPLICATIONS; ISOTOPES; LUMINESCENCE; MAMMALS; METALS; MONOSACCHARIDES; NEOPLASMS; NUCLEI; NUCLEOTIDES; ORGANIC COMPOUNDS; ORGANOIDS; RADIOISOTOPES; RODENTS; SACCHARIDES; SOMATIC CELLS; VERTEBRATES; 550201* - Biochemistry- Tracer Techniques

Citation Formats

Mohr, F C, and Fewtrell, C. The effect of mitochondrial inhibitors on calcium homeostasis in tumor mast cells. United States: N. p., 1990. Web.
Mohr, F C, & Fewtrell, C. The effect of mitochondrial inhibitors on calcium homeostasis in tumor mast cells. United States.
Mohr, F C, and Fewtrell, C. 1990. "The effect of mitochondrial inhibitors on calcium homeostasis in tumor mast cells". United States.
@article{osti_6995015,
title = {The effect of mitochondrial inhibitors on calcium homeostasis in tumor mast cells},
author = {Mohr, F C and Fewtrell, C},
abstractNote = {The depletion of intracellular ATP by mitochondrial inhibitors in a glucose-free saline solution inhibited antigen-stimulated 45Ca uptake, the rise in cytoplasmic calcium, measured by fura-2, and secretion in rat basophilic leukemia cells. Lowering the intracellular ATP concentration also released calcium from an intracellular store and made further 45Ca efflux from the cells unresponsive to subsequent antigen stimulation. Antigen-stimulated 45Ca efflux could be restored by the addition of glucose. The ATP-sensitive calcium store appeared to be the same store that releases calcium in response to antigen. In contrast, intracellular ATP was not lowered, and antigen-stimulated secretion was unaffected by mitochondrial inhibitors, provided that glucose was present in the bathing solution. Similarly, antigen-stimulated 45Ca uptake, 45Ca efflux, and the rise in free ionized calcium were unaffected by individual mitochondrial inhibitors in the presence of glucose. However, when the respiratory chain inhibitor antimycin A was used in combination with the ATP synthetase inhibitor oligomycin in the presence of glucose, antigen-stimulated 45Ca uptake was inhibited, whereas the rise in free ionized calcium and secretion were unaffected. Also, antigen-induced depolarization (an indirect measurement of Ca2+ influx across the plasma membrane) was not affected. The inhibition of antigen-stimulated 45Ca uptake could, however, be overcome if a high concentration of the Ca2+ buffer quin2 was present in the cells to buffer the incoming 45Ca. These results suggest that in fully functional rat basophilic leukemia cells the majority of the calcium entering in response to antigen stimulation is initially buffered by a calcium store sensitive to antimycin A and oligomycin, presumably the mitochondria.},
doi = {},
url = {https://www.osti.gov/biblio/6995015}, journal = {American Journal of Physiology; (USA)},
issn = {0002-9513},
number = ,
volume = 258,
place = {United States},
year = {Thu Feb 01 00:00:00 EST 1990},
month = {Thu Feb 01 00:00:00 EST 1990}
}