An in vitro model of arsine induced hemolysis and its application to possible treatments
| dc.contributor.advisor | Carter, Dean E. | en_US |
| dc.contributor.author | Shaver, Caryl Smith, 1959- | |
| dc.creator | Shaver, Caryl Smith, 1959- | en_US |
| dc.date.accessioned | 2013-04-03T13:08:27Z | |
| dc.date.available | 2013-04-03T13:08:27Z | |
| dc.date.issued | 1991 | en_US |
| dc.identifier.uri | http://hdl.handle.net/10150/277980 | |
| dc.description.abstract | Arsine gas is a potent hemolytic agent. Early work suggested glutathione depletion preceded, and oxygen required for hemolysis to occur. This study developed an in vitro model of arsine hemolysis, using the solubility of arsine gas in aqueous solutions. A total of 75% of the arsine was taken up into the cells within 5 minutes. Hemolysis occurred after 1-2 hours and reached 40-50%. Glutathione depletion occurred, but only after hemolysis reached its maximum. Increasing intracellular glutathione did not prevent hemolysis. The use of an intracellular chelator, monomethyldimercaptosuccinic acid did not prevent hemolysis. Hemolysis occurred in an oxygen excluding atmosphere but carboxyhemoglobin prevented hemolysis. Glutathione depletion is not a critical first step in arsine induced hemolysis. The interaction of arsine with the heme site of hemoglobin is critical to hemolysis. It is likely that a free radical intermediate of oxygen or arsine is the ultimate hemolytic agent. | |
| 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.title | An in vitro model of arsine induced hemolysis and its application to possible treatments | 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 | 1345620 | en_US |
| thesis.degree.discipline | Graduate College | en_US |
| thesis.degree.name | M.S. | en_US |
| dc.identifier.bibrecord | .b2705617x | en_US |
| refterms.dateFOA | 2018-08-19T08:32:13Z | |
| html.description.abstract | Arsine gas is a potent hemolytic agent. Early work suggested glutathione depletion preceded, and oxygen required for hemolysis to occur. This study developed an in vitro model of arsine hemolysis, using the solubility of arsine gas in aqueous solutions. A total of 75% of the arsine was taken up into the cells within 5 minutes. Hemolysis occurred after 1-2 hours and reached 40-50%. Glutathione depletion occurred, but only after hemolysis reached its maximum. Increasing intracellular glutathione did not prevent hemolysis. The use of an intracellular chelator, monomethyldimercaptosuccinic acid did not prevent hemolysis. Hemolysis occurred in an oxygen excluding atmosphere but carboxyhemoglobin prevented hemolysis. Glutathione depletion is not a critical first step in arsine induced hemolysis. The interaction of arsine with the heme site of hemoglobin is critical to hemolysis. It is likely that a free radical intermediate of oxygen or arsine is the ultimate hemolytic agent. |
