THE INVOLVEMENT OF RESPIRATION IN FREE-RADICAL PROCESSES DURING LOSS OF DESICCATION TOLERANCE IN GERMINATING ZEA-MAYS L - AN ELECTRON-PARAMAGNETIC-RESONANCE STUDY

Citation
O. Leprince et al., THE INVOLVEMENT OF RESPIRATION IN FREE-RADICAL PROCESSES DURING LOSS OF DESICCATION TOLERANCE IN GERMINATING ZEA-MAYS L - AN ELECTRON-PARAMAGNETIC-RESONANCE STUDY, Plant physiology, 104(4), 1994, pp. 1333-1339
Citations number
37
Categorie Soggetti
Plant Sciences
Journal title
ISSN journal
00320889
Volume
104
Issue
4
Year of publication
1994
Pages
1333 - 1339
Database
ISI
SICI code
0032-0889(1994)104:4<1333:TIORIF>2.0.ZU;2-#
Abstract
When germinating Zea mays L. seeds are rapidly desiccated, free radica l-mediated lipid peroxidation and phospholipid deesterification is acc ompanied by a desiccation-induced buildup of a stable free radical ass ociated with rapid loss of desiccation tolerance. Comparison of the el ectron paramagnetic resonance and electron nuclear double resonance pr operties of this radical with those of the radical in dried, desiccati on-intolerant moss showed that the two were identical. At the subcellu lar level, the radical was associated with the hydrophilic fraction re sulting from lipid extraction. Isolated mitochondria subjected to dryi ng were also found to accumulate an identical radical in vitro. When i ncreasing concentrations of cyanide were used, a significant positive correlation was shown between rates of respiration and the accumulatio n of the radical in desiccation-intolerant tissues. Another positive c orrelation was found when rates of O-2 uptake by radicles at different stages of germination were plotted against free radical content follo wing desiccation. This indicates that free radical production is close ly linked to respiration in a process likely to involve the desiccatio n-induced impairment of the mitochondrial electron transport chain to form thermodynamically favorable conditions to induce accumulation of a stable free radical and peroxidized lipids. Modulation of respiratio n using a range of inhibitors resulted in broadly similar modulation o f the buildup of the stable free radical. One site of radical generati on was likely to be the NADH dehydrogenase of complex I and probably a s a direct consequence of desiccation-impaired electron flow at or clo se to the ubiquinone pool.