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Jean-paul Viale - One of the best experts on this subject based on the ideXlab platform.
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Early septic shock induces loss of Oxidative Phosphorylation yield plasticity in liver mitochondria
Journal of Physiology and Biochemistry, 2014Co-Authors: Pierre Eyenga, Loïc Teulier, Damien Roussel, Jérôme Morel, Caroline Romestaing, Joëlle Goudable, Claude Negrier, Shey-shing Sheu, Jean-paul VialeAbstract:We aimed to study the change in mitochondrial Oxidative Phosphorylation efficiency occurring at the early stage of septic shock in an experimental model. Thirty-six male Wistar rats were divided into two groups. In the first group, a cecal ligation and puncture (CLP) was carried out to induce septic shock for 5 h. The second group includes sham-operated rats and constitutes the control group. Blood gas analysis, alanine amino transferase, and lactic acid dosages were assayed 5 h after surgery. Liver mitochondria were isolated for in vitro functional characterization, including mitochondrial respiratory parameters, Oxidative Phosphorylation efficiency, oxi-radical production, membrane potential, and cytochrome c oxidase activity and content. Liver interleukin 1β (IL-1β) and tumor necrosis α mRNA levels were determined. Septic shock induced a severe hypotension occurring 180 min after CLP in association with a metabolic acidosis, an increase in plasma alanine amino transferase, liver IL-1β gene expression, and mitochondrial reactive oxygen species production. The rates of mitochondrial oxygen consumption and the activity and content of cytochrome c oxidase were significantly decreased while no alterations in the Oxidative Phosphorylation efficiency and inner membrane integrity were found. These results show that contrary to what was expected, liver mitochondria felt to adjust their Oxidative Phosphorylation efficiency in response to the decrease in the mitochondrial Oxidative activity induced by CLP. This loss of mitochondrial bioenergetics plasticity might be related to mitochondrial Oxidative stress and liver cytokines production.
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Early septic shock induces loss of Oxidative Phosphorylation yield plasticity in liver mitochondria
Journal of Physiology and Biochemistry, 2014Co-Authors: Pierre Eyenga, Loïc Teulier, Damien Roussel, Jérôme Morel, Benjamin Rey, Caroline Romestaing, Sheu Shey-shing, Joëlle Goudable, Claude Negrier, Jean-paul VialeAbstract:We aimed to study the change in mitochondrial Oxidative Phosphorylation efficiency occurring at the early stage of septic shock in an experimental model. Thirty-six male Wistar rats were divided into two groups. In the first group, a cecal ligation and puncture (CLP) was carried out to induce septic shock for 5 h. The second group includes sham-operated rats and constitutes the control group. Blood gas analysis, alanine amino transferase, and lactic acid dosages were assayed 5 h after surgery. Liver mitochondria were isolated for in vitro functional characterization, including mitochondrial respiratory parameters, Oxidative Phosphorylation efficiency, oxi-radical production, membrane potential, and cytochrome c oxidase activity and content. Liver interleukin 1 beta (IL-1 beta) and tumor necrosis a mRNA levels were determined. Septic shock induced a severe hypotension occurring 180 min after CLP in association with a metabolic acidosis, an increase in plasma alanine amino transferase, liver IL-1 beta gene expression, and mitochondrial reactive oxygen species production. The rates of mitochondrial oxygen consumption and the activity and content of cytochrome c oxidase were significantly decreased while no alterations in the Oxidative Phosphorylation efficiency and inner membrane integrity were found. These results show that contrary to what was expected, liver mitochondria felt to adjust their Oxidative Phosphorylation efficiency in response to the decrease in the mitochondrial Oxidative activity induced by CLP. This loss of mitochondrial bioenergetics plasticity might be related to mitochondrial Oxidative stress and liver cytokines production.
Robert S Balaban - One of the best experts on this subject based on the ideXlab platform.
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effect of calcium on the Oxidative Phosphorylation cascade in skeletal muscle mitochondria
Biochemistry, 2013Co-Authors: Brian Glancy, Wayne T Willis, David J Chess, Robert S BalabanAbstract:Calcium is believed to regulate mitochondrial Oxidative Phosphorylation, thereby contributing to the maintenance of cellular energy homeostasis. Skeletal muscle, with an energy conversion dynamic range of up to 100-fold, is an extreme case for evaluating the cellular balance of ATP production and consumption. This study examined the role of Ca2+ in the entire Oxidative Phosphorylation reaction network in isolated skeletal muscle mitochondria and attempted to extrapolate these results back to the muscle, in vivo. Kinetic analysis was conducted to evaluate the dose–response effect of Ca2+ on the maximal velocity of Oxidative Phosphorylation (VmaxO) and the ADP affinity. Force-flow analysis evaluated the interplay between energetic driving forces and flux to determine the conductance, or effective activity, of individual steps within Oxidative Phosphorylation. Measured driving forces [extramitochondrial Phosphorylation potential (ΔGATP), membrane potential, and redox states of NADH and cytochromes bH, bL, c1...
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metabolic network control of Oxidative Phosphorylation multiple roles of inorganic phosphate
Journal of Biological Chemistry, 2003Co-Authors: Salil Bose, Stephanie French, Frank Evans, Fredric Joubert, Robert S BalabanAbstract:Abstract Phosphate (Pi) is a putative cytosolic signaling molecule in the regulation of Oxidative Phosphorylation. Here, by using a multiparameter monitoring system, we show that Pi controls Oxidative Phosphorylation in a balanced fashion, modulating both the generation of useful potential energy and the formation of ATP by F1F0-ATPase in heart and skeletal muscle mitochondria. In these studies the effect of Pi was determined on the mitochondria [NADH], NADH generating capacity, matrix pH, membrane potential, oxygen consumption, and cytochrome reduction level. Pi enhanced NADH generation and was obligatory for electron flow under uncoupled conditions. Pi oxidized cytochrome b (cyto-b) and reduced cytochrome c (cyto-c), potentially improving the coupling between the NADH free energy and the proton motive force. The apparent limitation in reducing equivalent flow between cyto-b and cyto-c in the absence of Pi was confirmed in the intact heart by using optical spectroscopic techniques under conditions with low cytosolic [Pi]. These results demonstrate that Pi signaling results in the balanced modulation of Oxidative Phosphorylation, by influencing both ΔGH+ generation and ATP production, which may contribute to the energy metabolism homeostasis observed in intact systems.
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Regulation of Oxidative Phosphorylation in the mammalian cell.
American Journal of Physiology-cell Physiology, 1990Co-Authors: Robert S BalabanAbstract:The cell is capable of maintaining a steady-state flux of energy from mitochondrial Oxidative Phosphorylation, producing ATP, to the cytosolic adenosinetriphosphatases (ATPases), performing work. C...
Pierre Eyenga - One of the best experts on this subject based on the ideXlab platform.
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Early septic shock induces loss of Oxidative Phosphorylation yield plasticity in liver mitochondria
Journal of Physiology and Biochemistry, 2014Co-Authors: Pierre Eyenga, Loïc Teulier, Damien Roussel, Jérôme Morel, Caroline Romestaing, Joëlle Goudable, Claude Negrier, Shey-shing Sheu, Jean-paul VialeAbstract:We aimed to study the change in mitochondrial Oxidative Phosphorylation efficiency occurring at the early stage of septic shock in an experimental model. Thirty-six male Wistar rats were divided into two groups. In the first group, a cecal ligation and puncture (CLP) was carried out to induce septic shock for 5 h. The second group includes sham-operated rats and constitutes the control group. Blood gas analysis, alanine amino transferase, and lactic acid dosages were assayed 5 h after surgery. Liver mitochondria were isolated for in vitro functional characterization, including mitochondrial respiratory parameters, Oxidative Phosphorylation efficiency, oxi-radical production, membrane potential, and cytochrome c oxidase activity and content. Liver interleukin 1β (IL-1β) and tumor necrosis α mRNA levels were determined. Septic shock induced a severe hypotension occurring 180 min after CLP in association with a metabolic acidosis, an increase in plasma alanine amino transferase, liver IL-1β gene expression, and mitochondrial reactive oxygen species production. The rates of mitochondrial oxygen consumption and the activity and content of cytochrome c oxidase were significantly decreased while no alterations in the Oxidative Phosphorylation efficiency and inner membrane integrity were found. These results show that contrary to what was expected, liver mitochondria felt to adjust their Oxidative Phosphorylation efficiency in response to the decrease in the mitochondrial Oxidative activity induced by CLP. This loss of mitochondrial bioenergetics plasticity might be related to mitochondrial Oxidative stress and liver cytokines production.
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Early septic shock induces loss of Oxidative Phosphorylation yield plasticity in liver mitochondria
Journal of Physiology and Biochemistry, 2014Co-Authors: Pierre Eyenga, Loïc Teulier, Damien Roussel, Jérôme Morel, Benjamin Rey, Caroline Romestaing, Sheu Shey-shing, Joëlle Goudable, Claude Negrier, Jean-paul VialeAbstract:We aimed to study the change in mitochondrial Oxidative Phosphorylation efficiency occurring at the early stage of septic shock in an experimental model. Thirty-six male Wistar rats were divided into two groups. In the first group, a cecal ligation and puncture (CLP) was carried out to induce septic shock for 5 h. The second group includes sham-operated rats and constitutes the control group. Blood gas analysis, alanine amino transferase, and lactic acid dosages were assayed 5 h after surgery. Liver mitochondria were isolated for in vitro functional characterization, including mitochondrial respiratory parameters, Oxidative Phosphorylation efficiency, oxi-radical production, membrane potential, and cytochrome c oxidase activity and content. Liver interleukin 1 beta (IL-1 beta) and tumor necrosis a mRNA levels were determined. Septic shock induced a severe hypotension occurring 180 min after CLP in association with a metabolic acidosis, an increase in plasma alanine amino transferase, liver IL-1 beta gene expression, and mitochondrial reactive oxygen species production. The rates of mitochondrial oxygen consumption and the activity and content of cytochrome c oxidase were significantly decreased while no alterations in the Oxidative Phosphorylation efficiency and inner membrane integrity were found. These results show that contrary to what was expected, liver mitochondria felt to adjust their Oxidative Phosphorylation efficiency in response to the decrease in the mitochondrial Oxidative activity induced by CLP. This loss of mitochondrial bioenergetics plasticity might be related to mitochondrial Oxidative stress and liver cytokines production.
Damien Roussel - One of the best experts on this subject based on the ideXlab platform.
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Early septic shock induces loss of Oxidative Phosphorylation yield plasticity in liver mitochondria
Journal of Physiology and Biochemistry, 2014Co-Authors: Pierre Eyenga, Loïc Teulier, Damien Roussel, Jérôme Morel, Caroline Romestaing, Joëlle Goudable, Claude Negrier, Shey-shing Sheu, Jean-paul VialeAbstract:We aimed to study the change in mitochondrial Oxidative Phosphorylation efficiency occurring at the early stage of septic shock in an experimental model. Thirty-six male Wistar rats were divided into two groups. In the first group, a cecal ligation and puncture (CLP) was carried out to induce septic shock for 5 h. The second group includes sham-operated rats and constitutes the control group. Blood gas analysis, alanine amino transferase, and lactic acid dosages were assayed 5 h after surgery. Liver mitochondria were isolated for in vitro functional characterization, including mitochondrial respiratory parameters, Oxidative Phosphorylation efficiency, oxi-radical production, membrane potential, and cytochrome c oxidase activity and content. Liver interleukin 1β (IL-1β) and tumor necrosis α mRNA levels were determined. Septic shock induced a severe hypotension occurring 180 min after CLP in association with a metabolic acidosis, an increase in plasma alanine amino transferase, liver IL-1β gene expression, and mitochondrial reactive oxygen species production. The rates of mitochondrial oxygen consumption and the activity and content of cytochrome c oxidase were significantly decreased while no alterations in the Oxidative Phosphorylation efficiency and inner membrane integrity were found. These results show that contrary to what was expected, liver mitochondria felt to adjust their Oxidative Phosphorylation efficiency in response to the decrease in the mitochondrial Oxidative activity induced by CLP. This loss of mitochondrial bioenergetics plasticity might be related to mitochondrial Oxidative stress and liver cytokines production.
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Early septic shock induces loss of Oxidative Phosphorylation yield plasticity in liver mitochondria
Journal of Physiology and Biochemistry, 2014Co-Authors: Pierre Eyenga, Loïc Teulier, Damien Roussel, Jérôme Morel, Benjamin Rey, Caroline Romestaing, Sheu Shey-shing, Joëlle Goudable, Claude Negrier, Jean-paul VialeAbstract:We aimed to study the change in mitochondrial Oxidative Phosphorylation efficiency occurring at the early stage of septic shock in an experimental model. Thirty-six male Wistar rats were divided into two groups. In the first group, a cecal ligation and puncture (CLP) was carried out to induce septic shock for 5 h. The second group includes sham-operated rats and constitutes the control group. Blood gas analysis, alanine amino transferase, and lactic acid dosages were assayed 5 h after surgery. Liver mitochondria were isolated for in vitro functional characterization, including mitochondrial respiratory parameters, Oxidative Phosphorylation efficiency, oxi-radical production, membrane potential, and cytochrome c oxidase activity and content. Liver interleukin 1 beta (IL-1 beta) and tumor necrosis a mRNA levels were determined. Septic shock induced a severe hypotension occurring 180 min after CLP in association with a metabolic acidosis, an increase in plasma alanine amino transferase, liver IL-1 beta gene expression, and mitochondrial reactive oxygen species production. The rates of mitochondrial oxygen consumption and the activity and content of cytochrome c oxidase were significantly decreased while no alterations in the Oxidative Phosphorylation efficiency and inner membrane integrity were found. These results show that contrary to what was expected, liver mitochondria felt to adjust their Oxidative Phosphorylation efficiency in response to the decrease in the mitochondrial Oxidative activity induced by CLP. This loss of mitochondrial bioenergetics plasticity might be related to mitochondrial Oxidative stress and liver cytokines production.
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Tissue variation of mitochondrial Oxidative Phosphorylation efficiency in cold-acclimated ducklings
Acta Biochimica Polonica, 2010Co-Authors: Karine Salin, Loïc Teulier, Jean-louis Rouanet, Yann Voituron, Claude Duchamp, Damien RousselAbstract:We investigated the Oxidative Phosphorylation efficiency of liver and gastrocnemius muscle mitochondria in thermoneutral and cold-acclimated ducklings. The yield of Oxidative Phosphorylation was lower in muscle than in liver mitochondria, a difference that was associated with a higher proton conductance in muscle mitochondria. Cold exposure did not affect Oxidative Phosphorylation efficiency or basal proton leak in mitochondria. We conclude that the basal proton conductance of mitochondria may regulate mitochondrial Oxidative Phosphorylation efficiency, but is not an important contributor to thermogenic processes in cold-acclimated ducklings.
Loïc Teulier - One of the best experts on this subject based on the ideXlab platform.
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Early septic shock induces loss of Oxidative Phosphorylation yield plasticity in liver mitochondria
Journal of Physiology and Biochemistry, 2014Co-Authors: Pierre Eyenga, Loïc Teulier, Damien Roussel, Jérôme Morel, Caroline Romestaing, Joëlle Goudable, Claude Negrier, Shey-shing Sheu, Jean-paul VialeAbstract:We aimed to study the change in mitochondrial Oxidative Phosphorylation efficiency occurring at the early stage of septic shock in an experimental model. Thirty-six male Wistar rats were divided into two groups. In the first group, a cecal ligation and puncture (CLP) was carried out to induce septic shock for 5 h. The second group includes sham-operated rats and constitutes the control group. Blood gas analysis, alanine amino transferase, and lactic acid dosages were assayed 5 h after surgery. Liver mitochondria were isolated for in vitro functional characterization, including mitochondrial respiratory parameters, Oxidative Phosphorylation efficiency, oxi-radical production, membrane potential, and cytochrome c oxidase activity and content. Liver interleukin 1β (IL-1β) and tumor necrosis α mRNA levels were determined. Septic shock induced a severe hypotension occurring 180 min after CLP in association with a metabolic acidosis, an increase in plasma alanine amino transferase, liver IL-1β gene expression, and mitochondrial reactive oxygen species production. The rates of mitochondrial oxygen consumption and the activity and content of cytochrome c oxidase were significantly decreased while no alterations in the Oxidative Phosphorylation efficiency and inner membrane integrity were found. These results show that contrary to what was expected, liver mitochondria felt to adjust their Oxidative Phosphorylation efficiency in response to the decrease in the mitochondrial Oxidative activity induced by CLP. This loss of mitochondrial bioenergetics plasticity might be related to mitochondrial Oxidative stress and liver cytokines production.
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Early septic shock induces loss of Oxidative Phosphorylation yield plasticity in liver mitochondria
Journal of Physiology and Biochemistry, 2014Co-Authors: Pierre Eyenga, Loïc Teulier, Damien Roussel, Jérôme Morel, Benjamin Rey, Caroline Romestaing, Sheu Shey-shing, Joëlle Goudable, Claude Negrier, Jean-paul VialeAbstract:We aimed to study the change in mitochondrial Oxidative Phosphorylation efficiency occurring at the early stage of septic shock in an experimental model. Thirty-six male Wistar rats were divided into two groups. In the first group, a cecal ligation and puncture (CLP) was carried out to induce septic shock for 5 h. The second group includes sham-operated rats and constitutes the control group. Blood gas analysis, alanine amino transferase, and lactic acid dosages were assayed 5 h after surgery. Liver mitochondria were isolated for in vitro functional characterization, including mitochondrial respiratory parameters, Oxidative Phosphorylation efficiency, oxi-radical production, membrane potential, and cytochrome c oxidase activity and content. Liver interleukin 1 beta (IL-1 beta) and tumor necrosis a mRNA levels were determined. Septic shock induced a severe hypotension occurring 180 min after CLP in association with a metabolic acidosis, an increase in plasma alanine amino transferase, liver IL-1 beta gene expression, and mitochondrial reactive oxygen species production. The rates of mitochondrial oxygen consumption and the activity and content of cytochrome c oxidase were significantly decreased while no alterations in the Oxidative Phosphorylation efficiency and inner membrane integrity were found. These results show that contrary to what was expected, liver mitochondria felt to adjust their Oxidative Phosphorylation efficiency in response to the decrease in the mitochondrial Oxidative activity induced by CLP. This loss of mitochondrial bioenergetics plasticity might be related to mitochondrial Oxidative stress and liver cytokines production.
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Tissue variation of mitochondrial Oxidative Phosphorylation efficiency in cold-acclimated ducklings
Acta Biochimica Polonica, 2010Co-Authors: Karine Salin, Loïc Teulier, Jean-louis Rouanet, Yann Voituron, Claude Duchamp, Damien RousselAbstract:We investigated the Oxidative Phosphorylation efficiency of liver and gastrocnemius muscle mitochondria in thermoneutral and cold-acclimated ducklings. The yield of Oxidative Phosphorylation was lower in muscle than in liver mitochondria, a difference that was associated with a higher proton conductance in muscle mitochondria. Cold exposure did not affect Oxidative Phosphorylation efficiency or basal proton leak in mitochondria. We conclude that the basal proton conductance of mitochondria may regulate mitochondrial Oxidative Phosphorylation efficiency, but is not an important contributor to thermogenic processes in cold-acclimated ducklings.
