Release of intracellular Calcium increase production of mitochondrial reactive oxygen species in renal distal epithelial cells

    Research output: Contribution to conferenceConference abstract for conferenceResearch

    Abstract

    Release of intracellular Calcium increase production of mitochondrial reactive oxygen species in renal distal epithelial cells.

    Henning F. Bjerregaard, Roskilde University, Department of Science, Systems and Models, 4000 Roskilde, Denmark. HFB@ RUC.DK

    Reactive oxygen species (ROS) like, hydrogen peroxide (H2O2) has traditionally been regarded as toxic by-products of aerobic metabolism. However, recent findings indicate that H2O2 act as a signalling molecule. The aim of the present study was to monitor, in real time, the rates of ROS generation in order to directly determine their production dynamics in living cells in response to hormonal signal events in the A6 cell culture. A6 cells have a divalent cation-sensing receptor (the extracellular calcium receptor) that can be stimulated with cadmium (Cd) and thereby induce a fast and transient liberation of calcium from intracellular stores, due to G-protein stimulation of phospholipase C and release of inositol -3 phosphate. Cd (0.4 mM) treatment of A6 cells enhanced the ROS production after one minutes incubation. The production rate was constant for at least 10 to 20 min. Experiments showed that the Cd induced increase in ROS production was inhibited by buffering of intracellular calcium with BAPTA, by the antioxidant N-acetylcysteine and by uncoupling of mitochondrial oxidative phosphorylation from respiration with CCCP. These results indicate that Cd generate a prompt initiation of ROS production from mitochondria due to an increase in the intracellular calcium concentration.

    Original languageEnglish
    Publication date2009
    Number of pages1
    Publication statusPublished - 2009
    Event36 th International Congress of Physiological Sciences - Kyoto, Japan
    Duration: 27 Jul 20091 Aug 2009

    Conference

    Conference36 th International Congress of Physiological Sciences
    CountryJapan
    CityKyoto
    Period27/07/200901/08/2009

    Cite this

    @conference{f5ea3560880311de9565000ea68e967b,
    title = "Release of intracellular Calcium increase production of mitochondrial reactive oxygen species in renal distal epithelial cells",
    abstract = "Release of intracellular Calcium increase production of mitochondrial reactive oxygen species in renal distal epithelial cells. Henning F. Bjerregaard, Roskilde University, Department of Science, Systems and Models, 4000 Roskilde, Denmark. HFB@ RUC.DKReactive oxygen species (ROS) like, hydrogen peroxide (H2O2) has traditionally been regarded as toxic by-products of aerobic metabolism. However, recent findings indicate that H2O2 act as a signalling molecule. The aim of the present study was to monitor, in real time, the rates of ROS generation in order to directly determine their production dynamics in living cells in response to hormonal signal events in the A6 cell culture. A6 cells have a divalent cation-sensing receptor (the extracellular calcium receptor) that can be stimulated with cadmium (Cd) and thereby induce a fast and transient liberation of calcium from intracellular stores, due to G-protein stimulation of phospholipase C and release of inositol -3 phosphate. Cd (0.4 mM) treatment of A6 cells enhanced the ROS production after one minutes incubation. The production rate was constant for at least 10 to 20 min. Experiments showed that the Cd induced increase in ROS production was inhibited by buffering of intracellular calcium with BAPTA, by the antioxidant N-acetylcysteine and by uncoupling of mitochondrial oxidative phosphorylation from respiration with CCCP. These results indicate that Cd generate a prompt initiation of ROS production from mitochondria due to an increase in the intracellular calcium concentration.",
    author = "Bjerregaard, {Henning F.}",
    year = "2009",
    language = "English",
    note = "null ; Conference date: 27-07-2009 Through 01-08-2009",

    }

    Release of intracellular Calcium increase production of mitochondrial reactive oxygen species in renal distal epithelial cells. / Bjerregaard, Henning F.

    2009. Abstract from 36 th International Congress of Physiological Sciences, Kyoto, Japan.

    Research output: Contribution to conferenceConference abstract for conferenceResearch

    TY - ABST

    T1 - Release of intracellular Calcium increase production of mitochondrial reactive oxygen species in renal distal epithelial cells

    AU - Bjerregaard, Henning F.

    PY - 2009

    Y1 - 2009

    N2 - Release of intracellular Calcium increase production of mitochondrial reactive oxygen species in renal distal epithelial cells. Henning F. Bjerregaard, Roskilde University, Department of Science, Systems and Models, 4000 Roskilde, Denmark. HFB@ RUC.DKReactive oxygen species (ROS) like, hydrogen peroxide (H2O2) has traditionally been regarded as toxic by-products of aerobic metabolism. However, recent findings indicate that H2O2 act as a signalling molecule. The aim of the present study was to monitor, in real time, the rates of ROS generation in order to directly determine their production dynamics in living cells in response to hormonal signal events in the A6 cell culture. A6 cells have a divalent cation-sensing receptor (the extracellular calcium receptor) that can be stimulated with cadmium (Cd) and thereby induce a fast and transient liberation of calcium from intracellular stores, due to G-protein stimulation of phospholipase C and release of inositol -3 phosphate. Cd (0.4 mM) treatment of A6 cells enhanced the ROS production after one minutes incubation. The production rate was constant for at least 10 to 20 min. Experiments showed that the Cd induced increase in ROS production was inhibited by buffering of intracellular calcium with BAPTA, by the antioxidant N-acetylcysteine and by uncoupling of mitochondrial oxidative phosphorylation from respiration with CCCP. These results indicate that Cd generate a prompt initiation of ROS production from mitochondria due to an increase in the intracellular calcium concentration.

    AB - Release of intracellular Calcium increase production of mitochondrial reactive oxygen species in renal distal epithelial cells. Henning F. Bjerregaard, Roskilde University, Department of Science, Systems and Models, 4000 Roskilde, Denmark. HFB@ RUC.DKReactive oxygen species (ROS) like, hydrogen peroxide (H2O2) has traditionally been regarded as toxic by-products of aerobic metabolism. However, recent findings indicate that H2O2 act as a signalling molecule. The aim of the present study was to monitor, in real time, the rates of ROS generation in order to directly determine their production dynamics in living cells in response to hormonal signal events in the A6 cell culture. A6 cells have a divalent cation-sensing receptor (the extracellular calcium receptor) that can be stimulated with cadmium (Cd) and thereby induce a fast and transient liberation of calcium from intracellular stores, due to G-protein stimulation of phospholipase C and release of inositol -3 phosphate. Cd (0.4 mM) treatment of A6 cells enhanced the ROS production after one minutes incubation. The production rate was constant for at least 10 to 20 min. Experiments showed that the Cd induced increase in ROS production was inhibited by buffering of intracellular calcium with BAPTA, by the antioxidant N-acetylcysteine and by uncoupling of mitochondrial oxidative phosphorylation from respiration with CCCP. These results indicate that Cd generate a prompt initiation of ROS production from mitochondria due to an increase in the intracellular calcium concentration.

    M3 - Conference abstract for conference

    ER -