MSpace - DSpace at UofM >
Faculty of Graduate Studies (Electronic Theses and Dissertations) >
FGS - Electronic Theses & Dissertations (Public) >

Please use this identifier to cite or link to this item: http://hdl.handle.net/1993/1221

Title: Regulation of polyglycerophospholipid biosynthesis
Authors: Ross, Timothy Kieran
Issue Date: 10-Oct-1998
Abstract: Cardiac ischaemia is a condition in which there exists an imbalance between the myocardial oxygen demand and coronary arterial supply. Biochemical complications arising from cardiac ischaemia include ATP depletion, a net loss of adenine nucleotides, as well as an increase in $\rm\lbrack Ca\sp{2+}$), (P$\sb{\rm i}\rbrack,$ and $\rm\lbrack H\sp+\rbrack.$ Ironically, cells may endure a non-lethal period of ischaemia, only to succumb to reperfusion injury. Reperfusion injury is a consequence of cell reoxygenation whereby the proliferation of oxygen free radicals (and resultant oxidative stress), increased $\rm\lbrack Ca\sp{2+}\rbrack,$ continued ATP deprivation, and higher pH all contribute to the reversible formation of a non-selective permeability transition pore in the inner mitochondrial membrane. The opening of this pore results in the further decoupling the cell's oxidative phosphorylation mechanisms, resulting in a vicious cycle of pore formation and decreased cellular metabolic efficiency. Cyclosporin A(CSA), an immunosuppressant, has been found to reverse pore formation in the post-ischaemic heart. Our goal was to study the effects of the opening and closing of these pores on cardiolipin biosynthesis. (Abstract shortened by UMI.)
URI: http://hdl.handle.net/1993/1221
Appears in Collection(s):FGS - Electronic Theses & Dissertations (Public)

Files in This Item:

File Description SizeFormat
MQ32238.pdf3.88 MBAdobe PDFView/Open
View Statistics

Items in MSpace are protected by copyright, with all rights reserved, unless otherwise indicated.

 

Valid XHTML 1.0! MSpace Software Copyright © 2002-2010  Duraspace - Feedback