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Impact of Post-Anoxia Stress on Membrane Lipids of Anoxia-Pretreated Potato Cells. A Re-Appraisal

Danijela Pavelic, Silvio Arpagaus, André Rawyler and Roland Brändle
Plant Physiology
Vol. 124, No. 3 (Nov., 2000), pp. 1285-1292
Stable URL: http://www.jstor.org/stable/4279530
Page Count: 8
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Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.
Impact of Post-Anoxia Stress on Membrane Lipids of Anoxia-Pretreated Potato Cells. A Re-Appraisal
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Abstract

The importance of lipid peroxidation and its contributing pathways (via reactive oxygen species and lipoxygenase) during post-anoxia was evaluated with respect to the biphasic behavior of membrane lipids under anoxia (A. Rawyler, D. Pavelic, C. Gianinazzi, J. Oberson, R. Brändle [1999] Plant Physiol 120: 293-300), using potato (Solanum tuberosum cv Bintje) cell cultures. When anoxic cells in the pre-lytic phase were re-oxygenated for 2 h, superoxide anion was not detectable, the hydrogen peroxide (H2O2) level remained small and similar to that of controls, and cell viability was preserved. Lipids were intact and no lipid hydroperoxides were detected. However, small amounts of lipid hydroperoxides accumulated upon feeding anoxic cells with H2O2 and incubation for an additional 2 h under anoxia. When cells that entered the lytic phase of anoxia were re-oxygenated for 2 h, the H2O2 and superoxide anion levels were essentially unchanged. However, cell respiration decreased, reflecting the extensive lipid hydrolysis that had already started under anoxia and continued during post-anoxia. Simultaneous with the massive release of free polyunsaturated fatty acids, small amounts of lipid hydroperoxides were formed, reaching 1% to 2% of total fatty acids. Catalase and superoxide dismutase activities were not greatly affected, whereas the amount and activity of lipoxygenase tended to increase during anoxia. Lipid peroxidation in potato cells is therefore low during post-anoxia. It is mainly due to lipoxygenase, whereas the contribution of reactive oxygen species is negligible. But above all, it is a late event that occurs only when irreversible damage is already caused by the anoxia-triggered lipid hydrolysis.

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