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Effect of H 2 O 2 on CCK‐8‐evoked changes in mitochondrial activity in isolated mouse pancreatic acinar cells
Author(s) -
Granados María P.,
Salido Ginés M.,
Pariente José A.,
González Antonio
Publication year - 2005
Publication title -
biology of the cell
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.543
H-Index - 85
eISSN - 1768-322X
pISSN - 0248-4900
DOI - 10.1042/bc20040513
Subject(s) - cholecystokinin , depolarization , mitochondrion , biology , cytosol , intracellular , autofluorescence , endocrinology , medicine , membrane potential , acinar cell , microbiology and biotechnology , pancreas , biochemistry , enzyme , fluorescence , physics , receptor , quantum mechanics
Background information . This paper studies the effect of H 2 O 2 on mitochondrial responses evoked by CCK‐8 (cholecystokinin 8) in mouse pancreatic acinar cells. Cytosolic ([Ca 2+ ] c ) and mitochondrial ([Ca 2+ ] m ) free‐calcium concentrations, mitochondrial inner membrane potential (ψ m ) and FAD autofluorescence were monitored using confocal laser scanning microscopy. Results . CCK‐8 induced an increase in [Ca 2+ ] m that slowly declined towards the prestimulation level. Depolarization of ψ m that partially recovered, as well as increases in FAD autofluorescence, could also be observed in response to the hormone. Pretreatment of cells with 1 mM H 2 O 2 alone resulted in marked changes in mitochondrial parameters and, moreover, H 2 O 2 inhibited the CCK‐8‐evoked changes in [Ca 2+ ] m , ψ m and FAD autofluorescence. The results of the present study have demonstrated that CCK‐8 can evoke marked changes in pancreatic acinar cell mitochondrial activity and that CCK‐8‐evoked responses are blocked by H 2 O 2 . Additionally, H 2 O 2 releases Ca 2+ from intracellular stores and inhibits pancreatic acinar cell responses to CCK‐8. Conclusion . The effects observed reflect an impairment of mitochondrial activity in the presence of H 2 O 2 that could represent some of its mechanisms of action to induce cellular damage leading to cell dysfunction and generation of pathologies.

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