Respiratory oscillations in yeast: mitochondrial reactive oxygen species, apoptosis and time; a hypothesis

Oscillatory metabolic activities occur more widely than is generally realised; detectability requires observation over extended times of single yeast cells or synchrony of individuals to provide a coherent population. Where oscillations in intracellular metabolite concentrations are observed, the ph...

Full description

Saved in:
Bibliographic Details
Published in:FEMS yeast research 2003-06, Vol.3 (4), p.333-339
Main Authors: Lloyd, David, Lemar, Katey M., Salgado, L.Eshantha J., Gould, Timothy M., Murray, Douglas B.
Format: Article
Language:English
Subjects:
Apoptosis
Apoptosis - physiology
Biological Clocks - physiology
Cell Respiration - physiology
Compartmentation
Hypotheses
Intracellular
Metabolites
Mitochondria
Mitochondria - metabolism
Mitochondria - physiology
Mitochondrion
Ordination
Oscillations
Oxidation-Reduction
Reactive oxygen
Reactive oxygen species
Reactive Oxygen Species - metabolism
Respiratory oscillation
Senescence
Ultradian clock
Yeasts - metabolism
Yeasts - physiology
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Oscillatory metabolic activities occur more widely than is generally realised; detectability requires observation over extended times of single yeast cells or synchrony of individuals to provide a coherent population. Where oscillations in intracellular metabolite concentrations are observed, the phenomenon has been ascribed to sloppy control, energetic optimisation, signalling, temporal compartmentation of incompatible reactions, or timekeeping functions. Here we emphasise the consequences of respiratory oscillations as a source of mitochondrially generated reactive O 2 metabolites. Temporal co-ordination of intracellular activities necessitates a time base. This is provided by an ultradian clock, and one result of its long-term operation is cyclic energisation of mitochondria, and thereby the generation of deleterious free radical species. Our hypothesis is that unrepaired cellular constituents and components (especially mitochondria) eventually lead to cellular senescence and apoptosis when a finite number of respiratory cycles has occurred.
ISSN:1567-1356
1567-1364
DOI:10.1016/S1567-1356(03)00071-0