Please use this identifier to cite or link to this item:
Title: Variations in spare electron transport chain capacity: The answer to an old riddle?
Authors: Fern, R
First Published: 15-Mar-2003
Citation: J NEUROSCI RES, 2003, 71 (6), pp. 759-762
Abstract: Several neurological diseases involve focal injury of specific brain structures. Poisons of the electron transport chain complexes (ETCC) can also produce selective injury of brain structures when given systemically and have been implicated in the development of neurological disease. Why ETCC poisons damage particular brain regions is unclear. Calculations of the relative ETCC expression level to glucose utilization rate (GUR) ratio from published observations here reveal that a low ETCC/GUR ratio predisposes a brain structure to injury by a poison of that complex. While GUR can rise with increased neuronal activity, ETCC expression is fixed in the short term. A high ETCC/GUR therefore represents surplus ETCC capacity, allowing for increased ATP generation with short-term increases in demand. A low ETCC/GUR indicates the opposite and will lead to energy failure when the specific ETCC is poisoned. These observations may explain why cyanide, a specific ETCC (IV) inhibitor, can produce selective injury of white matter, which has the lowest ETCC (IV)/GUR found in the brain. They are also consistent with the selective damage of the striatum produced by poisons such as rotenone, a form of injury implicated in Parkinson's disease. The striatum has a low ETCC (I)/GUR ratio, whereas rotenone is a selective ETCC (I) inhibitor.
DOI Link: 10.1002/jnr.10553
ISSN: 0360-4012
Type: Journal Article
Appears in Collections:Published Articles, Dept. of Cell Physiology and Pharmacology

Files in This Item:
There are no files associated with this item.

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