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Bernard Fromenty - One of the best experts on this subject based on the ideXlab platform.

  • Carbon tetrachloride-mediated Lipid Peroxidation induces early mitochondrial alterations in mouse liver.
    Laboratory Investigation, 2012
    Co-Authors: Laetitia Knockaert, A Berson, Catherine Ribault, Pierre-emmanuel Prost, Alain Fautrel, Julie Pajaud, Sylvie Lepage, Catherine Lucas-clerc, Jean-marc Bégué, Bernard Fromenty
    Abstract:

    Although carbon tetrachloride (CCl(4))-induced acute and chronic hepatotoxicity have been extensively studied, little is known about the very early in vivo effects of this organic solvent on oxidative stress and mitochondrial function. In this study, mice were treated with CCl(4) (1.5 ml/kg ie 2.38 g/kg) and parameters related to liver damage, Lipid Peroxidation, stress/defense and mitochondria were studied 3 h later. Some CCl(4)-intoxicated mice were also pretreated with the cytochrome P450 2E1 inhibitor diethyldithiocarbamate or the antioxidants Trolox C and dehydroepiandrosterone. CCl(4) induced a moderate elevation of aminotransferases, swelling of centrilobular hepatocytes, Lipid Peroxidation, reduction of cytochrome P4502E1 mRNA levels and a massive increase in mRNA expression of heme oxygenase-1 and heat shock protein 70. Moreover, CCl(4) intoxication induced a severe decrease of mitochondrial respiratory chain complex IV activity, mitochondrial DNA depletion and damage as well as ultrastructural alterations. Whereas DDTC totally or partially prevented all these hepatic toxic events, both antioxidants protected only against liver Lipid Peroxidation and mitochondrial damage. Taken together, our results suggest that Lipid Peroxidation is primarily implicated in CCl(4)-induced early mitochondrial injury. However, Lipid Peroxidation-independent mechanisms seem to be involved in CCl(4)-induced early hepatocyte swelling and changes in expression of stress/defense-related genes. Antioxidant therapy may not be an efficient strategy to block early liver damage after CCl(4) intoxication.

  • steatohepatitis inducing drugs cause mitochondrial dysfunction and Lipid Peroxidation in rat hepatocytes
    Gastroenterology, 1998
    Co-Authors: A Berson, Virginie De Beco, Philippe Letteron, Marie Robin, Claire Moreau, Johny El Kahwaji, Nicole Verthier, Gerard Feldmann, Bernard Fromenty, Dominique Pessayre
    Abstract:

    Abstract Background & Aims: 4,4'-Diethylaminoethoxyhexestrol (DEAEH), amiodarone, and perhexiline cause steatohepatitis in humans. The mechanisms of these effects are unknown for DEAEH and have not been completely elucidated for amiodarone and perhexiline. The aim of this study was to determine these mechanisms. Methods: Rat liver mitochondria, cultured rat hepatocytes, or rats were treated with these drugs, and the effects on mitochondrial respiration, β-oxidation, reactive oxygen species formation, and Lipid Peroxidation were determined. Results: DEAEH accumulated in mitochondria and inhibited carnitine palmitoyl transferase I and acyl–coenzyme A dehydrogenases; it decreased β-oxidation and caused Lipid deposits in hepatocytes. DEAEH also inhibited mitochondrial respiration and decreased adenosine triphosphate (ATP) levels in hepatocytes. DEAEH, amiodarone, and perhexiline augmented the mitochondrial formation of reactive oxygen species and caused Lipid Peroxidation in rats. Conclusions: Like amiodarone and perhexiline, DEAEH accumulates in mitochondria, where it inhibits both β-oxidation (causing steatosis) and respiration. Inhibition of respiration decreases ATP and also increases the mitochondrial formation of reactive oxygen species. The latter oxidize fat deposits, causing Lipid Peroxidation. We suggest that ATP depletion and Lipid Peroxidation may cause cell death and that Lipid Peroxidation products may account, in part, for other steatohepatitis lesions. GASTROENTEROLOGY 1998;114:764-774

  • steatohepatitis inducing drugs cause mitochondrial dysfunction and Lipid Peroxidation in rat hepatocytes
    Gastroenterology, 1998
    Co-Authors: A Berson, Virginie De Beco, Philippe Letteron, Marie Robin, Claire Moreau, Johny El Kahwaji, Nicole Verthier, Gerard Feldmann, Bernard Fromenty, Dominique Pessayre
    Abstract:

    Abstract Background & Aims: 4,4'-Diethylaminoethoxyhexestrol (DEAEH), amiodarone, and perhexiline cause steatohepatitis in humans. The mechanisms of these effects are unknown for DEAEH and have not been completely elucidated for amiodarone and perhexiline. The aim of this study was to determine these mechanisms. Methods: Rat liver mitochondria, cultured rat hepatocytes, or rats were treated with these drugs, and the effects on mitochondrial respiration, β-oxidation, reactive oxygen species formation, and Lipid Peroxidation were determined. Results: DEAEH accumulated in mitochondria and inhibited carnitine palmitoyl transferase I and acyl–coenzyme A dehydrogenases; it decreased β-oxidation and caused Lipid deposits in hepatocytes. DEAEH also inhibited mitochondrial respiration and decreased adenosine triphosphate (ATP) levels in hepatocytes. DEAEH, amiodarone, and perhexiline augmented the mitochondrial formation of reactive oxygen species and caused Lipid Peroxidation in rats. Conclusions: Like amiodarone and perhexiline, DEAEH accumulates in mitochondria, where it inhibits both β-oxidation (causing steatosis) and respiration. Inhibition of respiration decreases ATP and also increases the mitochondrial formation of reactive oxygen species. The latter oxidize fat deposits, causing Lipid Peroxidation. We suggest that ATP depletion and Lipid Peroxidation may cause cell death and that Lipid Peroxidation products may account, in part, for other steatohepatitis lesions. GASTROENTEROLOGY 1998;114:764-774

A Berson - One of the best experts on this subject based on the ideXlab platform.

  • Carbon tetrachloride-mediated Lipid Peroxidation induces early mitochondrial alterations in mouse liver.
    Laboratory Investigation, 2012
    Co-Authors: Laetitia Knockaert, A Berson, Catherine Ribault, Pierre-emmanuel Prost, Alain Fautrel, Julie Pajaud, Sylvie Lepage, Catherine Lucas-clerc, Jean-marc Bégué, Bernard Fromenty
    Abstract:

    Although carbon tetrachloride (CCl(4))-induced acute and chronic hepatotoxicity have been extensively studied, little is known about the very early in vivo effects of this organic solvent on oxidative stress and mitochondrial function. In this study, mice were treated with CCl(4) (1.5 ml/kg ie 2.38 g/kg) and parameters related to liver damage, Lipid Peroxidation, stress/defense and mitochondria were studied 3 h later. Some CCl(4)-intoxicated mice were also pretreated with the cytochrome P450 2E1 inhibitor diethyldithiocarbamate or the antioxidants Trolox C and dehydroepiandrosterone. CCl(4) induced a moderate elevation of aminotransferases, swelling of centrilobular hepatocytes, Lipid Peroxidation, reduction of cytochrome P4502E1 mRNA levels and a massive increase in mRNA expression of heme oxygenase-1 and heat shock protein 70. Moreover, CCl(4) intoxication induced a severe decrease of mitochondrial respiratory chain complex IV activity, mitochondrial DNA depletion and damage as well as ultrastructural alterations. Whereas DDTC totally or partially prevented all these hepatic toxic events, both antioxidants protected only against liver Lipid Peroxidation and mitochondrial damage. Taken together, our results suggest that Lipid Peroxidation is primarily implicated in CCl(4)-induced early mitochondrial injury. However, Lipid Peroxidation-independent mechanisms seem to be involved in CCl(4)-induced early hepatocyte swelling and changes in expression of stress/defense-related genes. Antioxidant therapy may not be an efficient strategy to block early liver damage after CCl(4) intoxication.

  • steatohepatitis inducing drugs cause mitochondrial dysfunction and Lipid Peroxidation in rat hepatocytes
    Gastroenterology, 1998
    Co-Authors: A Berson, Virginie De Beco, Philippe Letteron, Marie Robin, Claire Moreau, Johny El Kahwaji, Nicole Verthier, Gerard Feldmann, Bernard Fromenty, Dominique Pessayre
    Abstract:

    Abstract Background & Aims: 4,4'-Diethylaminoethoxyhexestrol (DEAEH), amiodarone, and perhexiline cause steatohepatitis in humans. The mechanisms of these effects are unknown for DEAEH and have not been completely elucidated for amiodarone and perhexiline. The aim of this study was to determine these mechanisms. Methods: Rat liver mitochondria, cultured rat hepatocytes, or rats were treated with these drugs, and the effects on mitochondrial respiration, β-oxidation, reactive oxygen species formation, and Lipid Peroxidation were determined. Results: DEAEH accumulated in mitochondria and inhibited carnitine palmitoyl transferase I and acyl–coenzyme A dehydrogenases; it decreased β-oxidation and caused Lipid deposits in hepatocytes. DEAEH also inhibited mitochondrial respiration and decreased adenosine triphosphate (ATP) levels in hepatocytes. DEAEH, amiodarone, and perhexiline augmented the mitochondrial formation of reactive oxygen species and caused Lipid Peroxidation in rats. Conclusions: Like amiodarone and perhexiline, DEAEH accumulates in mitochondria, where it inhibits both β-oxidation (causing steatosis) and respiration. Inhibition of respiration decreases ATP and also increases the mitochondrial formation of reactive oxygen species. The latter oxidize fat deposits, causing Lipid Peroxidation. We suggest that ATP depletion and Lipid Peroxidation may cause cell death and that Lipid Peroxidation products may account, in part, for other steatohepatitis lesions. GASTROENTEROLOGY 1998;114:764-774

  • steatohepatitis inducing drugs cause mitochondrial dysfunction and Lipid Peroxidation in rat hepatocytes
    Gastroenterology, 1998
    Co-Authors: A Berson, Virginie De Beco, Philippe Letteron, Marie Robin, Claire Moreau, Johny El Kahwaji, Nicole Verthier, Gerard Feldmann, Bernard Fromenty, Dominique Pessayre
    Abstract:

    Abstract Background & Aims: 4,4'-Diethylaminoethoxyhexestrol (DEAEH), amiodarone, and perhexiline cause steatohepatitis in humans. The mechanisms of these effects are unknown for DEAEH and have not been completely elucidated for amiodarone and perhexiline. The aim of this study was to determine these mechanisms. Methods: Rat liver mitochondria, cultured rat hepatocytes, or rats were treated with these drugs, and the effects on mitochondrial respiration, β-oxidation, reactive oxygen species formation, and Lipid Peroxidation were determined. Results: DEAEH accumulated in mitochondria and inhibited carnitine palmitoyl transferase I and acyl–coenzyme A dehydrogenases; it decreased β-oxidation and caused Lipid deposits in hepatocytes. DEAEH also inhibited mitochondrial respiration and decreased adenosine triphosphate (ATP) levels in hepatocytes. DEAEH, amiodarone, and perhexiline augmented the mitochondrial formation of reactive oxygen species and caused Lipid Peroxidation in rats. Conclusions: Like amiodarone and perhexiline, DEAEH accumulates in mitochondria, where it inhibits both β-oxidation (causing steatosis) and respiration. Inhibition of respiration decreases ATP and also increases the mitochondrial formation of reactive oxygen species. The latter oxidize fat deposits, causing Lipid Peroxidation. We suggest that ATP depletion and Lipid Peroxidation may cause cell death and that Lipid Peroxidation products may account, in part, for other steatohepatitis lesions. GASTROENTEROLOGY 1998;114:764-774

Dominique Pessayre - One of the best experts on this subject based on the ideXlab platform.

  • steatohepatitis inducing drugs cause mitochondrial dysfunction and Lipid Peroxidation in rat hepatocytes
    Gastroenterology, 1998
    Co-Authors: A Berson, Virginie De Beco, Philippe Letteron, Marie Robin, Claire Moreau, Johny El Kahwaji, Nicole Verthier, Gerard Feldmann, Bernard Fromenty, Dominique Pessayre
    Abstract:

    Abstract Background & Aims: 4,4'-Diethylaminoethoxyhexestrol (DEAEH), amiodarone, and perhexiline cause steatohepatitis in humans. The mechanisms of these effects are unknown for DEAEH and have not been completely elucidated for amiodarone and perhexiline. The aim of this study was to determine these mechanisms. Methods: Rat liver mitochondria, cultured rat hepatocytes, or rats were treated with these drugs, and the effects on mitochondrial respiration, β-oxidation, reactive oxygen species formation, and Lipid Peroxidation were determined. Results: DEAEH accumulated in mitochondria and inhibited carnitine palmitoyl transferase I and acyl–coenzyme A dehydrogenases; it decreased β-oxidation and caused Lipid deposits in hepatocytes. DEAEH also inhibited mitochondrial respiration and decreased adenosine triphosphate (ATP) levels in hepatocytes. DEAEH, amiodarone, and perhexiline augmented the mitochondrial formation of reactive oxygen species and caused Lipid Peroxidation in rats. Conclusions: Like amiodarone and perhexiline, DEAEH accumulates in mitochondria, where it inhibits both β-oxidation (causing steatosis) and respiration. Inhibition of respiration decreases ATP and also increases the mitochondrial formation of reactive oxygen species. The latter oxidize fat deposits, causing Lipid Peroxidation. We suggest that ATP depletion and Lipid Peroxidation may cause cell death and that Lipid Peroxidation products may account, in part, for other steatohepatitis lesions. GASTROENTEROLOGY 1998;114:764-774

  • steatohepatitis inducing drugs cause mitochondrial dysfunction and Lipid Peroxidation in rat hepatocytes
    Gastroenterology, 1998
    Co-Authors: A Berson, Virginie De Beco, Philippe Letteron, Marie Robin, Claire Moreau, Johny El Kahwaji, Nicole Verthier, Gerard Feldmann, Bernard Fromenty, Dominique Pessayre
    Abstract:

    Abstract Background & Aims: 4,4'-Diethylaminoethoxyhexestrol (DEAEH), amiodarone, and perhexiline cause steatohepatitis in humans. The mechanisms of these effects are unknown for DEAEH and have not been completely elucidated for amiodarone and perhexiline. The aim of this study was to determine these mechanisms. Methods: Rat liver mitochondria, cultured rat hepatocytes, or rats were treated with these drugs, and the effects on mitochondrial respiration, β-oxidation, reactive oxygen species formation, and Lipid Peroxidation were determined. Results: DEAEH accumulated in mitochondria and inhibited carnitine palmitoyl transferase I and acyl–coenzyme A dehydrogenases; it decreased β-oxidation and caused Lipid deposits in hepatocytes. DEAEH also inhibited mitochondrial respiration and decreased adenosine triphosphate (ATP) levels in hepatocytes. DEAEH, amiodarone, and perhexiline augmented the mitochondrial formation of reactive oxygen species and caused Lipid Peroxidation in rats. Conclusions: Like amiodarone and perhexiline, DEAEH accumulates in mitochondria, where it inhibits both β-oxidation (causing steatosis) and respiration. Inhibition of respiration decreases ATP and also increases the mitochondrial formation of reactive oxygen species. The latter oxidize fat deposits, causing Lipid Peroxidation. We suggest that ATP depletion and Lipid Peroxidation may cause cell death and that Lipid Peroxidation products may account, in part, for other steatohepatitis lesions. GASTROENTEROLOGY 1998;114:764-774

Daolin Tang - One of the best experts on this subject based on the ideXlab platform.

  • Lipid Peroxidation drives gasdermin d mediated pyroptosis in lethal polymicrobial sepsis
    Cell Host & Microbe, 2018
    Co-Authors: Rui Kang, Daolin Tang, Timothy R Billiar, Ling Zeng, Guido Kroemer, Haichao Wang, Jianxin Jiang
    Abstract:

    Summary Sepsis is a life-threatening condition caused by pathogen infection and associated with pyroptosis. Pyroptosis occurs upon activation of proinflammatory caspases and their subsequent cleavage of gasdermin D (GSDMD), resulting in GSDMD N-terminal fragments that form membrane pores to induce cell lysis. Here, we show that antioxidant defense enzyme glutathione peroxidase 4 (GPX4) and its ability to decrease Lipid Peroxidation, negatively regulate macrophage pyroptosis, and septic lethality in mice. Conditional Gpx4 knockout in myeloid lineage cells increases Lipid Peroxidation-dependent caspase-11 activation and GSDMD cleavage. The resultant N-terminal GSDMD fragments then trigger macrophage pyroptotic cell death in a phospholipase C gamma 1 (PLCG1)-dependent fashion. Administration of the antioxidant vitamin E that reduces Lipid Peroxidation, chemical inhibition of PLCG1, or genetic Caspase-11 deletion or Gsdmd inactivation prevents polymicrobial sepsis in Gpx4−/− mice. Collectively, this study suggests that Lipid Peroxidation drives GSDMD-mediated pyroptosis and hence constitutes a potential therapeutic target for lethal infection.

  • cisd1 inhibits ferroptosis by protection against mitochondrial Lipid Peroxidation
    Biochemical and Biophysical Research Communications, 2016
    Co-Authors: Hua Yuan, Rui Kang, Daolin Tang, Xiuying Zhang
    Abstract:

    Ferroptosis is a form of non-apoptotic cell death originally identified in cancer cells. However, the key regulator of ferroptosis in mitochondria remains unknown. Here, we show that CDGSH iron sulfur domain 1 (CISD1, also termed mitoNEET), an iron-containing outer mitochondrial membrane protein, negatively regulates ferroptotic cancer cell death. The classical ferroptosis inducer erastin promotes CISD1 expression in an iron-dependent manner in human hepatocellular carcinoma cells (e.g., HepG2 and Hep3B). Genetic inhibition of CISD1 increased iron-mediated intramitochondrial Lipid Peroxidation, which contributes to erastin-induced ferroptosis. In contrast, stabilization of the iron sulfur cluster of CISD1 by pioglitazone inhibits mitochondrial iron uptake, Lipid Peroxidation, and subsequent ferroptosis. These findings indicate a novel role of CISD1 in protecting against mitochondrial injury in ferroptosis.

Zhiyong Peng - One of the best experts on this subject based on the ideXlab platform.

  • reactive oxygen species induced Lipid Peroxidation in apoptosis autophagy and ferroptosis
    Oxidative Medicine and Cellular Longevity, 2019
    Co-Authors: Jiahao Zhang, Hernando Gomez, Raghavan Murugan, Xing Hong, Fan Jiang, Zhiyong Peng
    Abstract:

    Reactive oxygen species- (ROS-) induced Lipid Peroxidation plays a critical role in cell death including apoptosis, autophagy, and ferroptosis. This fundamental and conserved mechanism is based on an excess of ROS which attacks biomembranes, propagates Lipid Peroxidation chain reactions, and subsequently induces different types of cell death. A highly evolved sophisticated antioxidant system exists that acts to protect the cells from oxidative damage. In this review, we discussed how ROS propagate Lipid Peroxidation chain reactions and how the products of Lipid Peroxidation initiate apoptosis and autophagy in current models. We also discussed the mechanism of Lipid Peroxidation during ferroptosis, and we summarized Lipid Peroxidation in pathological conditions of critical illness. We aim to bring a more global and integrative sight to know how different ROS-induced Lipid Peroxidation occurs among apoptosis, autophagy, and ferroptosis.