Interactions of pentavalent and trivalent arsenic with intracellular thiols
dc.contributor.advisor | Carter, Dean E. | en_US |
dc.contributor.author | Winski, Shannon Lee, 1967- | |
dc.creator | Winski, Shannon Lee, 1967- | en_US |
dc.date.accessioned | 2013-04-03T13:11:13Z | |
dc.date.available | 2013-04-03T13:11:13Z | |
dc.date.issued | 1991 | en_US |
dc.identifier.uri | http://hdl.handle.net/10150/278054 | |
dc.description.abstract | Trivalent arsenic (As(III)) exposure is linked to cancer, but exposure includes pentavalent arsenic (As(V)). These forms interconvert in biological systems, and the mechanism is not understood. Arsenic has a high affinity for sulfhydryls, and the interaction of As(III) and As(V) with biological sulfhydryls and cellular uptake was investigated in this study. Incubation of rat blood at 1 mM arsenic showed As(V) uptake, membrane and protein binding to be time dependant. These processes were almost immediate with As(III) incubation. Incubation at 25 mM As(V) resulted in 40% thiol depletion with no oxidized glutathione formation. Metabolite analysis showed half of the As(V) converted to As(III). In As(III) incubation, 27% thiol depletion occurred with 300% increase in GSSG. As(V) reduction combined with thiol depletion could indicate that arsenate used sulfhydryls as reducing equivalents. Because arsenate uptake was slow this reduction may not be a main contributor to the overall in vivo process. | |
dc.language.iso | en_US | en_US |
dc.publisher | The University of Arizona. | en_US |
dc.rights | Copyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author. | en_US |
dc.subject | Health Sciences, Toxicology. | en_US |
dc.subject | Environmental Sciences. | en_US |
dc.title | Interactions of pentavalent and trivalent arsenic with intracellular thiols | en_US |
dc.type | text | en_US |
dc.type | Thesis-Reproduction (electronic) | en_US |
thesis.degree.grantor | University of Arizona | en_US |
thesis.degree.level | masters | en_US |
dc.identifier.proquest | 1346725 | en_US |
thesis.degree.discipline | Graduate College | en_US |
thesis.degree.name | M.S. | en_US |
dc.identifier.bibrecord | .b27253338 | en_US |
refterms.dateFOA | 2018-04-24T17:16:57Z | |
html.description.abstract | Trivalent arsenic (As(III)) exposure is linked to cancer, but exposure includes pentavalent arsenic (As(V)). These forms interconvert in biological systems, and the mechanism is not understood. Arsenic has a high affinity for sulfhydryls, and the interaction of As(III) and As(V) with biological sulfhydryls and cellular uptake was investigated in this study. Incubation of rat blood at 1 mM arsenic showed As(V) uptake, membrane and protein binding to be time dependant. These processes were almost immediate with As(III) incubation. Incubation at 25 mM As(V) resulted in 40% thiol depletion with no oxidized glutathione formation. Metabolite analysis showed half of the As(V) converted to As(III). In As(III) incubation, 27% thiol depletion occurred with 300% increase in GSSG. As(V) reduction combined with thiol depletion could indicate that arsenate used sulfhydryls as reducing equivalents. Because arsenate uptake was slow this reduction may not be a main contributor to the overall in vivo process. |