{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,28]],"date-time":"2026-02-28T13:31:32Z","timestamp":1772285492336,"version":"3.50.1"},"reference-count":31,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2011,12,22]],"date-time":"2011-12-22T00:00:00Z","timestamp":1324512000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Neuroscience Research"],"published-print":{"date-parts":[[2012,5]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>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<jats:sup>2+<\/jats:sup> deprivation and length of exposure to, and concentration of, oxidizing agents such as H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub> and thimerosal (TH). Cytosolic oxidation by 10 \u03bcM to 50 mM H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub> or 100 \u03bcM to 2 mM TH increases the probability of Ca<jats:sup>2+<\/jats:sup>\u2010dependent plasmalemmal sealing, whereas higher concentrations of H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub> 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\u201025, synaptobrevin, and N\u2010ethylmaleimide\u2010sensitive 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\u2010dependent neurodegenerative disorders, such as Parkinson's, Huntington's, and Alzheimer's diseases. \u00a9 2011 Wiley Periodicals, Inc.<\/jats:p>","DOI":"10.1002\/jnr.22823","type":"journal-article","created":{"date-parts":[[2011,12,23]],"date-time":"2011-12-23T04:47:59Z","timestamp":1324615679000},"page":"945-954","source":"Crossref","is-referenced-by-count":23,"title":["Neurite transection produces cytosolic oxidation, which enhances plasmalemmal repair"],"prefix":"10.1002","volume":"90","author":[{"given":"C.S.","family":"Spaeth","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"J.D.","family":"Fan","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"E.B.","family":"Spaeth","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"T.","family":"Robison","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"R.W.","family":"Wilcott","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"G.D.","family":"Bittner","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2011,12,22]]},"reference":[{"key":"e_1_2_6_2_1","first-page":"60","volume-title":"An introduction to categorical data analysis","author":"Agresti A","year":"1996"},{"key":"e_1_2_6_3_1","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.131.6.1747"},{"key":"e_1_2_6_4_1","first-page":"337","volume-title":"Axonal regeneration in the central nervous system","author":"Bittner GD","year":"2000"},{"key":"e_1_2_6_5_1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.76.1.514"},{"key":"e_1_2_6_6_1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M603952200"},{"key":"e_1_2_6_7_1","doi-asserted-by":"publisher","DOI":"10.1038\/ncb1812"},{"key":"e_1_2_6_8_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0197-0186(03)00101-3"},{"key":"e_1_2_6_9_1","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.18-20-08292.1998"},{"key":"e_1_2_6_10_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.neulet.2008.06.005"},{"key":"e_1_2_6_11_1","doi-asserted-by":"publisher","DOI":"10.1038\/labinvest.2010.36"},{"key":"e_1_2_6_12_1","doi-asserted-by":"publisher","DOI":"10.1002\/1097-4547(20001115)62:4<566::AID-JNR11>3.0.CO;2-4"},{"key":"e_1_2_6_13_1","doi-asserted-by":"publisher","DOI":"10.1038\/sj.jcbfm.9600399"},{"key":"e_1_2_6_14_1","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.129.1.105"},{"key":"e_1_2_6_15_1","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.3213-07.2008"},{"key":"e_1_2_6_16_1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.67.1.305"},{"key":"e_1_2_6_17_1","doi-asserted-by":"publisher","DOI":"10.1002\/j.1460-2075.1994.tb06834.x"},{"key":"e_1_2_6_18_1","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.4483-03.2004"},{"key":"e_1_2_6_19_1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M702582200"},{"key":"e_1_2_6_20_1","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.14-11-06638.1994"},{"key":"e_1_2_6_21_1","doi-asserted-by":"publisher","DOI":"10.1007\/s00401-010-0788-5"},{"key":"e_1_2_6_22_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.neulet.2010.03.078"},{"key":"e_1_2_6_23_1","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.200502031"},{"key":"e_1_2_6_24_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuroscience.2009.07.012"},{"key":"e_1_2_6_25_1","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.4155-10.2010"},{"key":"e_1_2_6_26_1","doi-asserted-by":"publisher","DOI":"10.1126\/science.7904084"},{"key":"e_1_2_6_27_1","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.22-01-00209.2002"},{"key":"e_1_2_6_28_1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M406327200"},{"key":"e_1_2_6_29_1","doi-asserted-by":"publisher","DOI":"10.1101\/gad.471708"},{"key":"e_1_2_6_30_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.mcn.2005.01.005"},{"key":"e_1_2_6_31_1","article-title":"Praoxonase\u20101 polymorphisms in Alzheimer's disease, Parkinson's disease, and AD\u2010PD spectrum diseases","author":"Wingo TS","year":"2010","journal-title":"Neurobiol Aging [E\u2010pub ahead of print]"},{"key":"e_1_2_6_32_1","doi-asserted-by":"publisher","DOI":"10.1002\/neu.20005"}],"container-title":["Journal of Neuroscience Research"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/api.wiley.com\/onlinelibrary\/tdm\/v1\/articles\/10.1002%2Fjnr.22823","content-type":"unspecified","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/onlinelibrary.wiley.com\/doi\/pdf\/10.1002\/jnr.22823","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,10,17]],"date-time":"2023-10-17T02:37:54Z","timestamp":1697510274000},"score":1,"resource":{"primary":{"URL":"https:\/\/onlinelibrary.wiley.com\/doi\/10.1002\/jnr.22823"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2011,12,22]]},"references-count":31,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2012,5]]}},"alternative-id":["10.1002\/jnr.22823"],"URL":"https:\/\/doi.org\/10.1002\/jnr.22823","archive":["Portico"],"relation":{},"ISSN":["0360-4012","1097-4547"],"issn-type":[{"value":"0360-4012","type":"print"},{"value":"1097-4547","type":"electronic"}],"subject":[],"published":{"date-parts":[[2011,12,22]]}}}