Cell damage caused by ATP depletion is reduced by magnesium and nickel in human fibroblasts--a non-specific calcium antagonism?
Autor: | Søren Risom Kristensen |
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Rok vydání: | 1991 |
Předmět: |
medicine.medical_specialty
Magnesium Chloride chemistry.chemical_element Calcium Cell Line Adenosine Triphosphate Nitrendipine Nickel Internal medicine Extracellular medicine Humans Fibroblast Molecular Biology Cell damage Edetic Acid L-Lactate Dehydrogenase Calcium channel Cell Biology Fibroblasts medicine.disease Kinetics medicine.anatomical_structure Endocrinology chemistry Biophysics Verapamil Antagonism medicine.drug |
Zdroj: | Biochimica et biophysica acta. 1091(3) |
ISSN: | 0006-3002 |
Popis: | Calcium has been suggested to be the final common mediator of cell damage, but conflicting reports to prove this hypothesis have appeared. In order to elucidate the role of calcium in cell damage caused by ATP depletion, the effect of addition of calcium channel blockers (verapamil and nitrendipine) and non-specific antagonists (magnesium and nickel) was investigated in a model system of quiescent fibroblasts. ATP depletion was induced by metabolic inhibitors and the cell damage was assessed by the release of lactate dehydrogenase. Verapamil and nitrendipine did not protect the cells during ATP depletion, whereas a high concentration of Mg 2+ (3–10 mmol/l) or a lower concentration of Ni 2+ (0.5–1.0 mmol/l) reduced the cell damage considerably. An increased extracellular concentration of Ca 2+ resulted in augmented cell damage. The effect of Mg 2+ and Ni 2+ was not due to an interference with the metabolic inhibitors or a reduction of the energy consumption. Both Ni 2+ and Mg 2+ were able to counteract the cell damage induced by entrance of Ca 2+ after addition of the ionophore A23187. However, Mg 2+ and Ni 2+ were deleterious for the cells during ATP regeneration after an initial ATP decrease. These results indicate that a non-specific antagonism of Ca 2+ may reduce cell damage, and, therefore, tha Ca 2+ may have an important role in cell damage, but also that a non-specific antagonism of Ca 2+ during regeneration of ATP depleted cells is deleterious. |
Databáze: | OpenAIRE |
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