The Experts below are selected from a list of 1584 Experts worldwide ranked by ideXlab platform

Jeffrey S. Armstrong - One of the best experts on this subject based on the ideXlab platform.

  • oltipraz induced phase 2 Enzyme response conserved in cells lacking mitochondrial dna
    Biochemical and Biophysical Research Communications, 2005
    Co-Authors: Yee Liu Chua, Dawei Zhang, Urs A Boelsterli, Philip K Moore, Matthew Whiteman, Jeffrey S. Armstrong
    Abstract:

    Oltipraz, a member of a class of 1,2-dithiolethiones, is a potent phase 2 Enzyme Inducing Agent used as a cancer chemopreventive. In this study, we investigated regulation of the phase 2 Enzyme response and protection against endogenous oxidative stress in lymphoblastic leukemic parental CEM cells and cells lacking mitochondrial DNA (mtDNA) (rho0) by oltipraz. Glutathione (GSH) levels (total and mitochondrial) and glutathione S-transferase (GST) activity were significantly increased after pretreatment with oltipraz in both parental (rho+) and rho0 cells, and both cell lines were resistant to mitochondrial oxidation, loss of mitochondrial membrane potential, and cell death in response to the GSH depleting Agent diethylmaleate. These results show that the phase 2 Enzyme response, by enhancing GSH-dependent systems involved in xenobiotic metabolism, blocks endogenous oxidative stress and cell death, and that this response is intact in cells lacking mtDNA.

Yee Liu Chua - One of the best experts on this subject based on the ideXlab platform.

  • oltipraz induced phase 2 Enzyme response conserved in cells lacking mitochondrial dna
    Biochemical and Biophysical Research Communications, 2005
    Co-Authors: Yee Liu Chua, Dawei Zhang, Urs A Boelsterli, Philip K Moore, Matthew Whiteman, Jeffrey S. Armstrong
    Abstract:

    Oltipraz, a member of a class of 1,2-dithiolethiones, is a potent phase 2 Enzyme Inducing Agent used as a cancer chemopreventive. In this study, we investigated regulation of the phase 2 Enzyme response and protection against endogenous oxidative stress in lymphoblastic leukemic parental CEM cells and cells lacking mitochondrial DNA (mtDNA) (rho0) by oltipraz. Glutathione (GSH) levels (total and mitochondrial) and glutathione S-transferase (GST) activity were significantly increased after pretreatment with oltipraz in both parental (rho+) and rho0 cells, and both cell lines were resistant to mitochondrial oxidation, loss of mitochondrial membrane potential, and cell death in response to the GSH depleting Agent diethylmaleate. These results show that the phase 2 Enzyme response, by enhancing GSH-dependent systems involved in xenobiotic metabolism, blocks endogenous oxidative stress and cell death, and that this response is intact in cells lacking mtDNA.

Dawei Zhang - One of the best experts on this subject based on the ideXlab platform.

  • oltipraz induced phase 2 Enzyme response conserved in cells lacking mitochondrial dna
    Biochemical and Biophysical Research Communications, 2005
    Co-Authors: Yee Liu Chua, Dawei Zhang, Urs A Boelsterli, Philip K Moore, Matthew Whiteman, Jeffrey S. Armstrong
    Abstract:

    Oltipraz, a member of a class of 1,2-dithiolethiones, is a potent phase 2 Enzyme Inducing Agent used as a cancer chemopreventive. In this study, we investigated regulation of the phase 2 Enzyme response and protection against endogenous oxidative stress in lymphoblastic leukemic parental CEM cells and cells lacking mitochondrial DNA (mtDNA) (rho0) by oltipraz. Glutathione (GSH) levels (total and mitochondrial) and glutathione S-transferase (GST) activity were significantly increased after pretreatment with oltipraz in both parental (rho+) and rho0 cells, and both cell lines were resistant to mitochondrial oxidation, loss of mitochondrial membrane potential, and cell death in response to the GSH depleting Agent diethylmaleate. These results show that the phase 2 Enzyme response, by enhancing GSH-dependent systems involved in xenobiotic metabolism, blocks endogenous oxidative stress and cell death, and that this response is intact in cells lacking mtDNA.

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

  • oltipraz induced phase 2 Enzyme response conserved in cells lacking mitochondrial dna
    Biochemical and Biophysical Research Communications, 2005
    Co-Authors: Yee Liu Chua, Dawei Zhang, Urs A Boelsterli, Philip K Moore, Matthew Whiteman, Jeffrey S. Armstrong
    Abstract:

    Oltipraz, a member of a class of 1,2-dithiolethiones, is a potent phase 2 Enzyme Inducing Agent used as a cancer chemopreventive. In this study, we investigated regulation of the phase 2 Enzyme response and protection against endogenous oxidative stress in lymphoblastic leukemic parental CEM cells and cells lacking mitochondrial DNA (mtDNA) (rho0) by oltipraz. Glutathione (GSH) levels (total and mitochondrial) and glutathione S-transferase (GST) activity were significantly increased after pretreatment with oltipraz in both parental (rho+) and rho0 cells, and both cell lines were resistant to mitochondrial oxidation, loss of mitochondrial membrane potential, and cell death in response to the GSH depleting Agent diethylmaleate. These results show that the phase 2 Enzyme response, by enhancing GSH-dependent systems involved in xenobiotic metabolism, blocks endogenous oxidative stress and cell death, and that this response is intact in cells lacking mtDNA.

Philip K Moore - One of the best experts on this subject based on the ideXlab platform.

  • oltipraz induced phase 2 Enzyme response conserved in cells lacking mitochondrial dna
    Biochemical and Biophysical Research Communications, 2005
    Co-Authors: Yee Liu Chua, Dawei Zhang, Urs A Boelsterli, Philip K Moore, Matthew Whiteman, Jeffrey S. Armstrong
    Abstract:

    Oltipraz, a member of a class of 1,2-dithiolethiones, is a potent phase 2 Enzyme Inducing Agent used as a cancer chemopreventive. In this study, we investigated regulation of the phase 2 Enzyme response and protection against endogenous oxidative stress in lymphoblastic leukemic parental CEM cells and cells lacking mitochondrial DNA (mtDNA) (rho0) by oltipraz. Glutathione (GSH) levels (total and mitochondrial) and glutathione S-transferase (GST) activity were significantly increased after pretreatment with oltipraz in both parental (rho+) and rho0 cells, and both cell lines were resistant to mitochondrial oxidation, loss of mitochondrial membrane potential, and cell death in response to the GSH depleting Agent diethylmaleate. These results show that the phase 2 Enzyme response, by enhancing GSH-dependent systems involved in xenobiotic metabolism, blocks endogenous oxidative stress and cell death, and that this response is intact in cells lacking mtDNA.