cytochrome-c-t and styrene-oxide

cytochrome-c-t has been researched along with styrene-oxide* in 1 studies

Other Studies

1 other study(ies) available for cytochrome-c-t and styrene-oxide

Article	Year
Styrene 7,8-oxide induces mitochondrial damage and oxidative stress in neurons. Toxicology, 2004, Sep-01, Volume: 201, Issue:1-3 Styrene 7,8-oxide (SO) is the main metabolite of styrene, a neurotoxic compound used industrially. Neurons exposed to SO undergo apoptosis with characteristic features including chromatin rearrangements and caspase activation. We report that the execution phase of apoptosis induced by SO (0.3 mM) in SK-N-MC neurons is triggered by translocation of apoptogenic factors (e.g., cytochrome c) into the cytosol. In addition, mitochondria exhibit lower Ca2+ capacity and loss of mitochondrial membrane potential (DeltaPsi). Lipid peroxidation, measured as thiobarbituric acid reactive substances (TBARS), is increased after 12 h. Pre-treatment with the antioxidant MnTBAP (100 microM) prevents the decrease of Ca2+ capacity, cytochrome c release, activation of caspases, exposure of phosphatidylserine and cell death. Hence, the neurotoxic effects of SO are related to mitochondrial damage and oxidative stress. Topics: Apoptosis; Calcium; Carcinogens; Cytochromes c; Epoxy Compounds; Humans; Membrane Potentials; Mitochondria; Neurons; Oxidative Stress; Reactive Oxygen Species; Thiobarbituric Acid Reactive Substances; Tumor Cells, Cultured	2004

Article

Year

Styrene 7,8-oxide induces mitochondrial damage and oxidative stress in neurons.

Toxicology, 2004, Sep-01, Volume: 201, Issue:1-3

Styrene 7,8-oxide (SO) is the main metabolite of styrene, a neurotoxic compound used industrially. Neurons exposed to SO undergo apoptosis with characteristic features including chromatin rearrangements and caspase activation. We report that the execution phase of apoptosis induced by SO (0.3 mM) in SK-N-MC neurons is triggered by translocation of apoptogenic factors (e.g., cytochrome c) into the cytosol. In addition, mitochondria exhibit lower Ca2+ capacity and loss of mitochondrial membrane potential (DeltaPsi). Lipid peroxidation, measured as thiobarbituric acid reactive substances (TBARS), is increased after 12 h. Pre-treatment with the antioxidant MnTBAP (100 microM) prevents the decrease of Ca2+ capacity, cytochrome c release, activation of caspases, exposure of phosphatidylserine and cell death. Hence, the neurotoxic effects of SO are related to mitochondrial damage and oxidative stress.

Topics: Apoptosis; Calcium; Carcinogens; Cytochromes c; Epoxy Compounds; Humans; Membrane Potentials; Mitochondria; Neurons; Oxidative Stress; Reactive Oxygen Species; Thiobarbituric Acid Reactive Substances; Tumor Cells, Cultured

2004