Neurite transection produces cytosolic oxidation, which enhances plasmalemmal repair

To survive, cells must rapidly repair (seal) plasmalemmal damage. Cytosolic oxidation has been shown to increase cell survival in some cases and produce cell death in other protocols. An antioxidant (melatonin; Mel) has been reported to decrease the probability of sealing plasmalemmal damage. Here w...

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Published in:	Journal of neuroscience research Vol. 90; no. 5; pp. 945 - 954
Main Authors:	Spaeth, C.S., Fan, J.D., Spaeth, E.B., Robison, T., Wilcott, R.W., Bittner, G.D.
Format:	Journal Article
Language:	English
Published:	Hoboken Wiley Subscription Services, Inc., A Wiley Company 01-05-2012
Subjects:	Animals Antioxidants - pharmacology axonal repair Axotomy B104 cells calcium Calcium - metabolism Cell Line, Tumor Cell Membrane - drug effects Cell Membrane - physiology Cytosol - drug effects Cytosol - physiology Dose-Response Relationship, Drug Drug Interactions H2O2 Hydrogen Peroxide - pharmacology melatonin methylene blue neurite transection Neurites - drug effects Neurites - metabolism Neuroblastoma - pathology Oxidants - pharmacology oxidation Oxidation-Reduction - drug effects plasmalemmal damage Protein Kinase Inhibitors - pharmacology Rats Time Factors Wound Healing - drug effects Wound Healing - physiology
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Abstract	To survive, cells must rapidly repair (seal) plasmalemmal damage. Cytosolic oxidation has been shown to increase cell survival in some cases and produce cell death in other protocols. An antioxidant (melatonin; Mel) has been reported to decrease the probability of sealing plasmalemmal damage. Here we report that plasmalemmal damage produces cytosolic oxidation, as assayed by methylene blue (MB) color change in rat B104 hippocampal cells. Plasmalemmal sealing is affected by duration of Ca2+ deprivation and length of exposure to, and concentration of, oxidizing agents such as H2O2 and thimerosal (TH). Cytosolic oxidation by 10 μM to 50 mM H2O2 or 100 μM to 2 mM TH increases the probability of Ca2+‐dependent plasmalemmal sealing, whereas higher concentrations of H2O2 decrease sealing probability and also damage uninjured cells. We also show that antioxidants (Mel, MB) or reducing agents (dithiothreitol) decrease sealing. Proteins, such as protein kinase A, SNAP‐25, synaptobrevin, and N‐ethylmaleimide‐sensitive factor (previously reported to enhance sealing in other pathways), also enhance sealing in this oxidation pathway. In brief, our data show that plasmalemmal damage produces cytosolic oxidation that increases the probability of plasmalemmal sealing, which is strongly correlated with cell survival in other studies. Our results may provide new insights into the etiology and treatment of oxidation‐dependent neurodegenerative disorders, such as Parkinson's, Huntington's, and Alzheimer's diseases. © 2011 Wiley Periodicals, Inc.
AbstractList	To survive, cells must rapidly repair (seal) plasmalemmal damage. Cytosolic oxidation has been shown to increase cell survival in some cases and produce cell death in other protocols. An antioxidant (melatonin; Mel) has been reported to decrease the probability of sealing plasmalemmal damage. Here we report that plasmalemmal damage produces cytosolic oxidation, as assayed by methylene blue (MB) color change in rat B104 hippocampal cells. Plasmalemmal sealing is affected by duration of Ca²⁺ deprivation and length of exposure to, and concentration of, oxidizing agents such as H₂O₂ and thimerosal (TH). Cytosolic oxidation by 10 μM to 50 mM H₂O₂ or 100 μM to 2 mM TH increases the probability of Ca²⁺-dependent plasmalemmal sealing, whereas higher concentrations of H₂O₂ decrease sealing probability and also damage uninjured cells. We also show that antioxidants (Mel, MB) or reducing agents (dithiothreitol) decrease sealing. Proteins, such as protein kinase A, SNAP-25, synaptobrevin, and N-ethylmaleimide-sensitive factor (previously reported to enhance sealing in other pathways), also enhance sealing in this oxidation pathway. In brief, our data show that plasmalemmal damage produces cytosolic oxidation that increases the probability of plasmalemmal sealing, which is strongly correlated with cell survival in other studies. Our results may provide new insights into the etiology and treatment of oxidation-dependent neurodegenerative disorders, such as Parkinson's, Huntington's, and Alzheimer's diseases. To survive, cells must rapidly repair (seal) plasmalemmal damage. Cytosolic oxidation has been shown to increase cell survival in some cases and produce cell death in other protocols. An antioxidant (melatonin; Mel) has been reported to decrease the probability of sealing plasmalemmal damage. Here we report that plasmalemmal damage produces cytosolic oxidation, as assayed by methylene blue (MB) color change in rat B104 hippocampal cells. Plasmalemmal sealing is affected by duration of Ca2+ deprivation and length of exposure to, and concentration of, oxidizing agents such as H2O2 and thimerosal (TH). Cytosolic oxidation by 10 μM to 50 mM H2O2 or 100 μM to 2 mM TH increases the probability of Ca2+‐dependent plasmalemmal sealing, whereas higher concentrations of H2O2 decrease sealing probability and also damage uninjured cells. We also show that antioxidants (Mel, MB) or reducing agents (dithiothreitol) decrease sealing. Proteins, such as protein kinase A, SNAP‐25, synaptobrevin, and N‐ethylmaleimide‐sensitive factor (previously reported to enhance sealing in other pathways), also enhance sealing in this oxidation pathway. In brief, our data show that plasmalemmal damage produces cytosolic oxidation that increases the probability of plasmalemmal sealing, which is strongly correlated with cell survival in other studies. Our results may provide new insights into the etiology and treatment of oxidation‐dependent neurodegenerative disorders, such as Parkinson's, Huntington's, and Alzheimer's diseases. © 2011 Wiley Periodicals, Inc. To survive, cells must rapidly repair (seal) plasmalemmal damage. Cytosolic oxidation has been shown to increase cell survival in some cases and produce cell death in other protocols. An antioxidant (melatonin; Mel) has been reported to decrease the probability of sealing plasmalemmal damage. Here we report that plasmalemmal damage produces cytosolic oxidation, as assayed by methylene blue (MB) color change in rat B104 hippocampal cells. Plasmalemmal sealing is affected by duration of Ca 2+ deprivation and length of exposure to, and concentration of, oxidizing agents such as H 2 O 2 and thimerosal (TH). Cytosolic oxidation by 10 μM to 50 mM H 2 O 2 or 100 μM to 2 mM TH increases the probability of Ca 2+ ‐dependent plasmalemmal sealing, whereas higher concentrations of H 2 O 2 decrease sealing probability and also damage uninjured cells. We also show that antioxidants (Mel, MB) or reducing agents (dithiothreitol) decrease sealing. Proteins, such as protein kinase A, SNAP‐25, synaptobrevin, and N‐ethylmaleimide‐sensitive factor (previously reported to enhance sealing in other pathways), also enhance sealing in this oxidation pathway. In brief, our data show that plasmalemmal damage produces cytosolic oxidation that increases the probability of plasmalemmal sealing, which is strongly correlated with cell survival in other studies. Our results may provide new insights into the etiology and treatment of oxidation‐dependent neurodegenerative disorders, such as Parkinson's, Huntington's, and Alzheimer's diseases. © 2011 Wiley Periodicals, Inc.
Author	Bittner, G.D. Robison, T. Fan, J.D. Spaeth, C.S. Spaeth, E.B. Wilcott, R.W.
Author_xml	– sequence: 1 givenname: C.S. surname: Spaeth fullname: Spaeth, C.S. organization: Institute for Cellular and Molecular Biology, University of Texas at Austin, Austin, Texas – sequence: 2 givenname: J.D. surname: Fan fullname: Fan, J.D. organization: Section of Neurobiology, University of Texas at Austin, Austin, Texas – sequence: 3 givenname: E.B. surname: Spaeth fullname: Spaeth, E.B. organization: Section of Neurobiology, University of Texas at Austin, Austin, Texas – sequence: 4 givenname: T. surname: Robison fullname: Robison, T. organization: Section of Neurobiology, University of Texas at Austin, Austin, Texas – sequence: 5 givenname: R.W. surname: Wilcott fullname: Wilcott, R.W. organization: Section of Neurobiology, University of Texas at Austin, Austin, Texas – sequence: 6 givenname: G.D. surname: Bittner fullname: Bittner, G.D. email: bittner@mail.utexas.edu organization: Institute for Cellular and Molecular Biology, University of Texas at Austin, Austin, Texas
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/22497022$$D View this record in MEDLINE/PubMed
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Copyright	Copyright © 2011 Wiley Periodicals, Inc. Copyright © 2012 Wiley Periodicals, Inc.
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Snippet	To survive, cells must rapidly repair (seal) plasmalemmal damage. Cytosolic oxidation has been shown to increase cell survival in some cases and produce cell...
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SubjectTerms	Animals Antioxidants - pharmacology axonal repair Axotomy B104 cells calcium Calcium - metabolism Cell Line, Tumor Cell Membrane - drug effects Cell Membrane - physiology Cytosol - drug effects Cytosol - physiology Dose-Response Relationship, Drug Drug Interactions H2O2 Hydrogen Peroxide - pharmacology melatonin methylene blue neurite transection Neurites - drug effects Neurites - metabolism Neuroblastoma - pathology Oxidants - pharmacology oxidation Oxidation-Reduction - drug effects plasmalemmal damage Protein Kinase Inhibitors - pharmacology Rats Time Factors Wound Healing - drug effects Wound Healing - physiology
Title	Neurite transection produces cytosolic oxidation, which enhances plasmalemmal repair
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