Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
6143083 | Virus Research | 2012 | 12 Pages |
Abstract
⺠Extracellular HIV-1 Vpr induces a decline in astrocytic ATP and GSH levels. ⺠Exogenous HIV-1 Vpr promotes accumulation of reactive oxygen species. ⺠N-acetyl-cysteine treatment ameliorates HIV-1 Vpr-induced oxidative stress. ⺠Exposure of astrocytes to HIV-1 Vpr increases levels of oxidized glutathione. ⺠Treatment with HIV-1 Vpr disrupts primary astrocytes architectural structure.
Keywords
BSOGSSGDAPINACHEKGSTGSH4F2hcxCTPBShemaglutinin4′,6-diamidino-2-phenylindoleN-acetyl-cysteineROSSDS–PAGEVprAdenosine TriphosphateATPAstrocytessodium dodecyl sulfate–polyacrylamide gel electrophoresisbuthionine sulfoximineOxidative stressCNScentral nervous systemPhosphate-buffered salinepolymerase chain reactionPCRHIV-1Human immunodeficiency virus type 1reduced glutathioneGlutathioneglutathione S-transferaseoxidized glutathioneReactive oxygen species
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Authors
Adriano Ferrucci, Michael R. Nonnemacher, Ãric A. Cohen, Brian Wigdahl,