An in vitro model of arsine induced hemolysis and its application to possible treatments

Persistent Link:
http://hdl.handle.net/10150/277980
Title:
An in vitro model of arsine induced hemolysis and its application to possible treatments
Author:
Shaver, Caryl Smith, 1959-
Issue Date:
1991
Publisher:
The University of Arizona.
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.
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.
Type:
text; Thesis-Reproduction (electronic)
Keywords:
Health Sciences, Toxicology.
Degree Name:
M.S.
Degree Level:
masters
Degree Program:
Graduate College
Degree Grantor:
University of Arizona
Advisor:
Carter, Dean E.

Full metadata record

DC FieldValue Language
dc.language.isoen_USen_US
dc.titleAn in vitro model of arsine induced hemolysis and its application to possible treatmentsen_US
dc.creatorShaver, Caryl Smith, 1959-en_US
dc.contributor.authorShaver, Caryl Smith, 1959-en_US
dc.date.issued1991en_US
dc.publisherThe University of Arizona.en_US
dc.rightsCopyright © 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.description.abstractArsine 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.en_US
dc.typetexten_US
dc.typeThesis-Reproduction (electronic)en_US
dc.subjectHealth Sciences, Toxicology.en_US
thesis.degree.nameM.S.en_US
thesis.degree.levelmastersen_US
thesis.degree.disciplineGraduate Collegeen_US
thesis.degree.grantorUniversity of Arizonaen_US
dc.contributor.advisorCarter, Dean E.en_US
dc.identifier.proquest1345620en_US
dc.identifier.bibrecord.b2705617xen_US
All Items in UA Campus Repository are protected by copyright, with all rights reserved, unless otherwise indicated.