Regulation of polyglycerophospholipid biosynthesis
| dc.contributor.author | Ross, Timothy Kieran | en_US |
| dc.date.accessioned | 2007-05-15T19:06:04Z | |
| dc.date.available | 2007-05-15T19:06:04Z | |
| dc.date.issued | 1998-10-10T00:00:00Z | en_US |
| dc.degree.discipline | Biochemistry | en_US |
| dc.degree.level | Master of Science (M.Sc.) | en_US |
| dc.description.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.) | en_US |
| dc.format.extent | 3977035 bytes | |
| dc.format.extent | 184 bytes | |
| dc.format.mimetype | application/pdf | |
| dc.format.mimetype | text/plain | |
| dc.identifier.uri | http://hdl.handle.net/1993/1221 | |
| dc.language.iso | eng | en_US |
| dc.rights | open access | en_US |
| dc.title | Regulation of polyglycerophospholipid biosynthesis | en_US |
| dc.type | master thesis | en_US |