F Morscher1, I Kranner1, E Arc1, C Bailly2, T Roach3. 1. Institute of Botany, Leopold-Franzens-Universität-Innsbruck, Sternwartestraße 15, 6020 Innsbruck, Austria and. 2. Sorbonne Universités, UPMC Univ Paris 06, Institut de Biologie Paris-Seine (IBPS), UMR 7622, F-75005 Paris, France and CNRS, IBPS, UMR 7622, Biologie du développement, F-75005 Paris, France. 3. Institute of Botany, Leopold-Franzens-Universität-Innsbruck, Sternwartestraße 15, 6020 Innsbruck, Austria and thomas.roach@uibk.ac.at.
Abstract
BACKGROUND AND AIMS: Loss of seed viability has been associated with deteriorative processes that are partly caused by oxidative damage. The breaking of dormancy, a seed trait that prevents germination in unfavourable seasons, has also been associated with oxidative processes. It is neither clear how much overlap exists between these mechanisms nor is the specific roles played by oxygen and reactive oxygen species. METHODS: Antioxidant profiles were studied in fresh (dormant) or after-ripened (non-dormant) sunflower (Helianthus annuus) embryos subjected to controlled deterioration at 40 °C and 75 % relative humidity under ambient (21 %) or high O2 (75 %). Changes in seed vigour and viability, dormancy, protein carbonylation and fatty acid composition were also studied. KEY RESULTS: After-ripening of embryonic axes was accompanied by a shift in the thiol-based cellular redox environment towards more oxidizing conditions. Controlled deterioration under high O2 led to a faster loss of seed dormancy and significant decreases in glutathione reductase and glutathione peroxidase activities, but viability was lost at the same rate as under ambient O2. Irrespective of O2 concentration, the overall thiol-based cellular redox state increased significantly over 21 d of controlled deterioration to strongly oxidizing conditions and then plateaued, while viability continued to decrease. Viability loss was accompanied by a rapid decrease in glucose-6-phosphate-dehydrogenase, which provides NADPH for reductive processes such as required by glutathione reductase. Protein carbonylation, a marker of protein oxidation, increased strongly in deteriorating seeds. The lipid-soluble tocochromanols, dominated by α-tocopherol, and fatty acid profiles remained stable. CONCLUSIONS: After-ripening, dormancy-breaking during ageing and viability loss appeared to be associated with oxidative changes of the cytosolic environment and proteins in the embryonic axis rather than the lipid environment. High O2 concentrations accelerated dormancy alleviation but, surprisingly, did not accelerate the rate of viability loss.
BACKGROUND AND AIMS: Loss of seed viability has been associated with deteriorative processes that are partly caused by oxidative damage. The breaking of dormancy, a seed trait that prevents germination in unfavourable seasons, has also been associated with oxidative processes. It is neither clear how much overlap exists between these mechanisms nor is the specific roles played by oxygen and reactive oxygen species. METHODS: Antioxidant profiles were studied in fresh (dormant) or after-ripened (non-dormant) sunflower (Helianthus annuus) embryos subjected to controlled deterioration at 40 °C and 75 % relative humidity under ambient (21 %) or high O2 (75 %). Changes in seed vigour and viability, dormancy, protein carbonylation and fatty acid composition were also studied. KEY RESULTS: After-ripening of embryonic axes was accompanied by a shift in the thiol-based cellular redox environment towards more oxidizing conditions. Controlled deterioration under high O2 led to a faster loss of seed dormancy and significant decreases in glutathione reductase and glutathione peroxidase activities, but viability was lost at the same rate as under ambient O2. Irrespective of O2 concentration, the overall thiol-based cellular redox state increased significantly over 21 d of controlled deterioration to strongly oxidizing conditions and then plateaued, while viability continued to decrease. Viability loss was accompanied by a rapid decrease in glucose-6-phosphate-dehydrogenase, which provides NADPH for reductive processes such as required by glutathione reductase. Protein carbonylation, a marker of protein oxidation, increased strongly in deteriorating seeds. The lipid-soluble tocochromanols, dominated by α-tocopherol, and fatty acid profiles remained stable. CONCLUSIONS: After-ripening, dormancy-breaking during ageing and viability loss appeared to be associated with oxidative changes of the cytosolic environment and proteins in the embryonic axis rather than the lipid environment. High O2 concentrations accelerated dormancy alleviation but, surprisingly, did not accelerate the rate of viability loss.
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