Cytotoxicity of an organic hydroperoxide and cellular antioxidant defense system against hydroperoxides in cultured mammalian cells

Oxidative Stress in a Clonal Cell Line of Neuronal Origin: Effects of Antioxidant Enzyme Modulation

“…A sixfold lower basal GPx activity has been reported in the mouse neuroblastoma line N 18, in which activity can be increased 23-fold by incubation 6 days with 60 nM selenite (Germain and Arneson, 1977). In addition to the N18 line, selenite-dependent stimulation of GPx activity up to 10-fold has been reported in a number of nonneuronal cell lines including several human tumor lines (Sandstrom et al, 1987), hamster fibroblasts (Ochi and Miyaura, 1989), and bovine adrenocortical cultures (Hornsby et al, 1985). In all cases, maximum stimulation was achieved using selenite concentrations and incubation times similar to those in the present investigation.…”

Oxidative Stress in a Clonal Cell Line of Neuronal Origin: Effects of Antioxidant Enzyme Modulation

“…A sixfold lower basal GPx activity has been reported in the mouse neuroblastoma line N 18, in which activity can be increased 23-fold by incubation 6 days with 60 nM selenite (Germain and Arneson, 1977). In addition to the N18 line, selenite-dependent stimulation of GPx activity up to 10-fold has been reported in a number of nonneuronal cell lines including several human tumor lines (Sandstrom et al, 1987), hamster fibroblasts (Ochi and Miyaura, 1989), and bovine adrenocortical cultures (Hornsby et al, 1985). In all cases, maximum stimulation was achieved using selenite concentrations and incubation times similar to those in the present investigation.…”

Influence of different chemical agents (H2O2, t-BHP and MMS) on the activity of antioxidant enzymes in human HepG2 and hamster V79 cells; relationship to cytotoxicity and genotoxicity

“…The activities of GPx were in V79 cells reduced mainly at lower concentrations. Selective inhibition of GPx (without effect on glutathione reductase activity) was described in t-BHP-treated V79 cells also by Ochi and Miyaura [10]. These authors observed t-BHP-induced depletion of glutathione (GSH, a radical scavenger) causing increased cytotoxicity in V79 cells.…”

Mechanism for the changes in levels of glutathione upon exposure of cultured mammalian cells to tertiary-butylhydroperoxide and diamide

“…These observations appear to demonstrate a difference between the mechanism for the decrease in levels of total GSH and that for the increase in levels of GSSG by t-BuOOH. Reactive oxygen radicals appear to be involved in the decrease in levels of total GSH that is caused by t-BuOOH, as was also the case in earlier studies in which either o-phenanthroline or the trivalent-iron chelator desferrioxamine suppressed the induction by t-BuOOH of cytotoxicity (Ochi 1988;Ochi and Miyaura 1989), DNA single-strand breaks Muhlematter et al 1989), and chromosomal aberrations (Ochi 1989). However, the increase in levels of GSSG caused by t-BuOOH seems not to be attributable to the action of reactive oxygen radicals but to be a result of oxidation of GSH by unchanged t-BuOOH.…”

“…Experimental design used here was the same as used in earlier studies for the inductions by t-BuOOH of cytostatic effect (Ochi and Miyaura 1989), repairable DNA singlestrand breaks and chromosomal aberrations (Ochi 1989) and the reversible inhibition of the activity of GSH peroxidase (Ochi 1990). Therefore, the rapid increase in levels of GSH after exposure to t-BuOOH may be a cellular response comparable to the repairs against the cellular and molecular changes induced by the hydroperoxide as described above.…”

Oxidative Stress in a Clonal Cell Line of Neuronal Origin: Effects of Antioxidant Enzyme Modulation

“…A sixfold lower basal GPx activity has been reported in the mouse neuroblastoma line N 18, in which activity can be increased 23-fold by incubation 6 days with 60 nM selenite (Germain and Arneson, 1977). In addition to the N18 line, selenite-dependent stimulation of GPx activity up to 10-fold has been reported in a number of nonneuronal cell lines including several human tumor lines (Sandstrom et al, 1987), hamster fibroblasts (Ochi and Miyaura, 1989), and bovine adrenocortical cultures (Hornsby et al, 1985). In all cases, maximum stimulation was achieved using selenite concentrations and incubation times similar to those in the present investigation.…”

Influence of different chemical agents (H2O2, t-BHP and MMS) on the activity of antioxidant enzymes in human HepG2 and hamster V79 cells; relationship to cytotoxicity and genotoxicity

“…The activities of GPx were in V79 cells reduced mainly at lower concentrations. Selective inhibition of GPx (without effect on glutathione reductase activity) was described in t-BHP-treated V79 cells also by Ochi and Miyaura [10]. These authors observed t-BHP-induced depletion of glutathione (GSH, a radical scavenger) causing increased cytotoxicity in V79 cells.…”

Mechanism for the changes in levels of glutathione upon exposure of cultured mammalian cells to tertiary-butylhydroperoxide and diamide

“…These observations appear to demonstrate a difference between the mechanism for the decrease in levels of total GSH and that for the increase in levels of GSSG by t-BuOOH. Reactive oxygen radicals appear to be involved in the decrease in levels of total GSH that is caused by t-BuOOH, as was also the case in earlier studies in which either o-phenanthroline or the trivalent-iron chelator desferrioxamine suppressed the induction by t-BuOOH of cytotoxicity (Ochi 1988;Ochi and Miyaura 1989), DNA single-strand breaks Muhlematter et al 1989), and chromosomal aberrations (Ochi 1989). However, the increase in levels of GSSG caused by t-BuOOH seems not to be attributable to the action of reactive oxygen radicals but to be a result of oxidation of GSH by unchanged t-BuOOH.…”

“…Experimental design used here was the same as used in earlier studies for the inductions by t-BuOOH of cytostatic effect (Ochi and Miyaura 1989), repairable DNA singlestrand breaks and chromosomal aberrations (Ochi 1989) and the reversible inhibition of the activity of GSH peroxidase (Ochi 1990). Therefore, the rapid increase in levels of GSH after exposure to t-BuOOH may be a cellular response comparable to the repairs against the cellular and molecular changes induced by the hydroperoxide as described above.…”

Oxidative Stress in a Clonal Cell Line of Neuronal Origin: Effects of Antioxidant Enzyme Modulation

“…A sixfold lower basal GPx activity has been reported in the mouse neuroblastoma line N 18, in which activity can be increased 23-fold by incubation 6 days with 60 nM selenite (Germain and Arneson, 1977). In addition to the N18 line, selenite-dependent stimulation of GPx activity up to 10-fold has been reported in a number of nonneuronal cell lines including several human tumor lines (Sandstrom et al, 1987), hamster fibroblasts (Ochi and Miyaura, 1989), and bovine adrenocortical cultures (Hornsby et al, 1985). In all cases, maximum stimulation was achieved using selenite concentrations and incubation times similar to those in the present investigation.…”

Influence of different chemical agents (H2O2, t-BHP and MMS) on the activity of antioxidant enzymes in human HepG2 and hamster V79 cells; relationship to cytotoxicity and genotoxicity

“…The activities of GPx were in V79 cells reduced mainly at lower concentrations. Selective inhibition of GPx (without effect on glutathione reductase activity) was described in t-BHP-treated V79 cells also by Ochi and Miyaura [10]. These authors observed t-BHP-induced depletion of glutathione (GSH, a radical scavenger) causing increased cytotoxicity in V79 cells.…”

Mechanism for the changes in levels of glutathione upon exposure of cultured mammalian cells to tertiary-butylhydroperoxide and diamide

“…These observations appear to demonstrate a difference between the mechanism for the decrease in levels of total GSH and that for the increase in levels of GSSG by t-BuOOH. Reactive oxygen radicals appear to be involved in the decrease in levels of total GSH that is caused by t-BuOOH, as was also the case in earlier studies in which either o-phenanthroline or the trivalent-iron chelator desferrioxamine suppressed the induction by t-BuOOH of cytotoxicity (Ochi 1988;Ochi and Miyaura 1989), DNA single-strand breaks Muhlematter et al 1989), and chromosomal aberrations (Ochi 1989). However, the increase in levels of GSSG caused by t-BuOOH seems not to be attributable to the action of reactive oxygen radicals but to be a result of oxidation of GSH by unchanged t-BuOOH.…”

“…Experimental design used here was the same as used in earlier studies for the inductions by t-BuOOH of cytostatic effect (Ochi and Miyaura 1989), repairable DNA singlestrand breaks and chromosomal aberrations (Ochi 1989) and the reversible inhibition of the activity of GSH peroxidase (Ochi 1990). Therefore, the rapid increase in levels of GSH after exposure to t-BuOOH may be a cellular response comparable to the repairs against the cellular and molecular changes induced by the hydroperoxide as described above.…”