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Hardly Increased Oxidative Stress After Exposure to Low Temperature in Chilling‐Acclimated and Non‐Acclimated Maize Leaves
Author(s) -
Leipner J.,
Basilidès A.,
Stamp P.,
Fracheboud Y.
Publication year - 2000
Publication title -
plant biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.871
H-Index - 87
eISSN - 1438-8677
pISSN - 1435-8603
DOI - 10.1055/s-2000-13919
Subject(s) - xanthophyll , catalase , photosynthesis , photosystem ii , antioxidant , hydrogen peroxide , biology , photosystem i , reactive oxygen species , oxidative stress , botany , superoxide dismutase , carotenoid , horticulture , biochemistry
Seedlings of Zea mays L. were grown at optimal (25 °C) and suboptimal (15 °C) temperature and then exposed to severe chilling temperature (6 °C) at their growth light intensity (450 ìmol quanta m −2 s −1 ) for 4 d. Photosynthetic parameters, hydrogen peroxide, antioxidant contents, and activity of scavenging enzymes were investigated before, during, and after chilling stress. This stress caused a stronger reduction in photosynthetic activity, maximum quantum efficiency of photosystem II primary photochemistry ( F v / F m ), and catalase activity in plants which had been grown at 25 °C rather than at 15 °C. Maize plants grown at suboptimal temperature de‐epoxidized their xanthophyll cycle pool to a greater extent and exhibited a faster recovery from chilling stress than plants which had not been acclimated to chilling. Antioxidant content, activity of scavenging enzymes, with the exception of catalase, hydrogen peroxide formation, and the size of the xanthophyll cycle pool were hardly affected by chilling stress. However, chilling induced a temporary increase in the glutathione content and triggered the synthesis of á‐tocopherol during the phase of recovery at 25 °C. The results indicate that leaves respond to chilling stress by down‐regulation of photosystem II accompanied by de‐epoxidation of the xanthophyll cycle pool, probably to prevent enhanced formation of superoxide radicals at photosystem I and, consequently, other reactive oxygen species.