The Production of a Reactive Oxygen Intermediate during the Induction of Apoptosis by Cytotoxic Insult

McGowan, Adrian J.; Bowie, Andrew; O’Neill, Luke A.J.; Cotter, Thomas G.

doi:10.1006/excr.1997.3853

Cited by 36 publications

(18 citation statements)

References 56 publications

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“…The change in DCF fluorescence, which is indicative of oxidative stress, may thus be due to increased production of ROS, to a decreased capacity of antioxidant defence mechanisms, or to both. The increased activity of NADPH oxidases seems to be a major source of ROS in HL-60 cells and U937 human leukaemic cells induced to apoptosis by irradiation with UV light and by treatment with camptothecin (McGowan et al, 1998). Most of the oxygen taken up by non-myeloid cells is consumed by mitochondria, and 1-2 % of the oxygen consumed by mitochondria is reduced to superoxide anion radicals in the respiratory chain (Richter & Schweizer, 1997).…”

Section: Discussionmentioning

confidence: 99%

Oxidative stress in cells infected with bovine viral diarrhoea virus: a crucial step in the induction of apoptosis.

Schweizer

Peterhans

1999

Journal of General Virology

102

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Bovine viral diarrhoea virus (BVDV) belongs to the genus Pestivirus of the family Flaviviridae. Both a noncytopathic (ncp) and an antigenically related cytopathic (cp) BVDV can be isolated from persistently infected animals suffering from mucosal disease. In every case studied so far, the genomic changes leading to the cp biotype correlate with the production of the NS3 nonstructural protein, which, in the ncp biotype, is present in its uncleaved form, NS23. This report shows that, in contrast to ncp BVDV, the cp biotype induces apoptosis in cultured embryonic bovine turbinate cells. Early in the process of apoptosis, cells show a rise in the intracellular level of reactive oxygen species, which is indicative of oxidative stress. This precedes two hallmarks of apoptosis, caspase activation as shown by cleavage of the caspase substrate poly(ADP-ribose) polymerase, and DNA fragmentation. Cells were protected from apoptosis only by certain antioxidants (butylated hydroxyanisole and ebselen), whereas others (N-acetylcysteine, pyrrolidine dithiocarbamate, lipoic acid, dihydrolipoic acid and tiron) turned out to be ineffective. Antioxidants that protected cells from apoptosis prevented oxidative stress but failed to block virus growth. These observations suggest that oxidative stress, which occurs early in the interaction between cp BVDV and its host cell, may be a crucial event in the sequence leading to apoptotic cell death. Hence, apoptosis is not required for the multiplication of the cp biotype of BVDV.

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Section: Discussionmentioning

confidence: 99%

Oxidative stress in cells infected with bovine viral diarrhoea virus: a crucial step in the induction of apoptosis.

Schweizer

Peterhans

1999

Journal of General Virology

102

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“…In contrast to the apoptosis triggering role of reactive oxygen species observed in several cell systems 5,6 superoxide anion functions as a natural inhibitor of Fas mediated cell death. 7 Hydrogen peroxide has been also observed to delay Fas mediated apoptosis.…”

Section: Introductionmentioning

confidence: 86%

Fas mediated apoptosis of human Jurkat T-cells: intracellular events and potentiation by redox-active α-lipoic acid

1999

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Activation of caspases is required in Fas receptor mediated apoptosis. Maintenance of a reducing environment inside the cell has been suggested to be necessary for caspase activity during apoptosis. We explored the possibility to potentiate Fas mediated killing of tumor cells by a-lipoic acid (LA), a redox-active drug and nutrient that is intracellularly reduced to a potent reductant dihydrolipoic acid. Treatment of cells with 100 mM LA for 72 h markedly potentiated Fas-mediated apoptosis of leukemic Jurkat cells but not that of peripheral blood lymphocytes from healthy humans. In Jurkat, Fas activation was followed by rapid loss of cell thiols, decreased mitochondrial membrane potential, increased [Ca 2+ ] i and increased PKC activity; all these responses were potentiated in LA pretreated cells. PKCd played an important role in mediating the effect of LA on Fas-mediated cell death. In response to Fas activation LA treatment potentiated caspase 3 activation by over 100%. The ability of LA to potentiate Fas mediated killing of leukemic cells was abrogated by a caspase 3 inhibitor suggesting that increased caspase 3 activity in LAtreated Fas-activated cells played an important role in potentiating cell death. This work provides first evidence showing that inducible caspase 3 activity may be pharmacologically up-regulated by reducing agents such as dihydrolipoic acid.

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“…[43][44][45][46] Incomplete reversal of leukemic cell death by the antioxidant NAC suggests that FTY720 most likely has multiple effects culminating in cellular toxicity and ultimately cell death. ROS can be generated in apoptotic and nonapoptotic modes of cell death.…”

confidence: 99%

FTY720 produces caspase-independent cell death of acute lymphoblastic leukemia cells

Wallington-Beddoe¹,

Hewson²,

Bradstock³

et al. 2011

Autophagy

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The Production of a Reactive Oxygen Intermediate during the Induction of Apoptosis by Cytotoxic Insult

Cited by 36 publications

References 56 publications

Oxidative stress in cells infected with bovine viral diarrhoea virus: a crucial step in the induction of apoptosis.

Oxidative stress in cells infected with bovine viral diarrhoea virus: a crucial step in the induction of apoptosis.

Fas mediated apoptosis of human Jurkat T-cells: intracellular events and potentiation by redox-active α-lipoic acid

FTY720 produces caspase-independent cell death of acute lymphoblastic leukemia cells

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