STRESS TOLERANCE AND MEMBRANE LIPID UNSATURATION IN SACCHAROMYCES-CEREVISIAE GROWN AEROBICALLY OR ANAEROBICALLY

Citation
El. Steels et al., STRESS TOLERANCE AND MEMBRANE LIPID UNSATURATION IN SACCHAROMYCES-CEREVISIAE GROWN AEROBICALLY OR ANAEROBICALLY, Microbiology, 140, 1994, pp. 569-576
Citations number
36
Categorie Soggetti
Microbiology
Journal title
ISSN journal
13500872
Volume
140
Year of publication
1994
Part
3
Pages
569 - 576
Database
ISI
SICI code
1350-0872(1994)140:<569:STAMLU>2.0.ZU;2-Y
Abstract
Saccharomyces cerevisiae cells grown either aerobically or anaerobical ly were tested for tolerance to a brief heat stress (52 degrees C, 5 m in) or oxidative stress (20 mM H2O2, 15 min). Tolerance was related to growth phase. in that stationary phase cells were intrinsically more resistant to heat or oxidative stress than exponential phase cells. A mild heat shock (37 degrees C, 30 min) induced thermotolerance and oxi dative tolerance in both aerobic and anaerobic cells. However, prior e xposure to a low concentration of H2O2 (0.1 mM, 60 min) induced protec tion against the lethal concentration of H2O2 but not against the leth al temperature. Sensitivity to both heat and oxidative stress was depe ndent on membrane lipid composition. In the case of anaerobic cells, t he most stress resistant had membranes enriched in saturated fatty aci ds, followed in order by cells enriched in oleic and linolenic acids. Aerobic cells with membranes enriched in palmitoleic and oleic acids s howed the highest resistance to stress under all conditions. In both a erobic and anaerobic cells, a mild heat shock or oxidative shock induc ed markedly increased levels of thiobarbituric acid reactive substance (TBARS), indicative of malondialdehyde formation and lipid damage. An aerobic cells with membranes enriched in linolenic acid had the highes t TBARS, followed by cells enriched in oleic acid, with cells enriched in saturated fatty acids showing the lowest TBARS. The results sugges t that heat and oxidative stress may share a common mechanism of damag e through induction of oxygen-derived free radicals, resulting in memb rane lipid damage. The extent of cellular damage was related to membra ne lipid composition and correlated positively with increasing unsatur ation of the phospholipid fatty acyl component.