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Detoxification function of aldose/aldehyde reductase during drought and ultraviolet‐B (280–320 nm) stresses
Author(s) -
HIDEG É.,
NAGY T.,
OBERSCHALL A.,
DUDITS D.,
VASS I.
Publication year - 2003
Publication title -
plant, cell and environment
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.646
H-Index - 200
eISSN - 1365-3040
pISSN - 0140-7791
DOI - 10.1046/j.1365-3040.2003.00982.x
Subject(s) - tbars , lipid peroxidation , reactive oxygen species , aldose reductase , chemistry , biochemistry , aldehyde dehydrogenase , oxidative stress , thiobarbituric acid , aldehyde reductase , photoinhibition , enzyme , food science , horticulture , biology , photosynthesis , photosystem ii
Plants may activate similar defence systems to reduce cellular damages caused by different stress conditions. In the present experiments, the formation of lipid peroxidation products [thiobarbituric acid reactive species (TBARS)] was significant during both drought and ultraviolet (UV)‐B stresses, whereas the formation of reactive oxygen species (ROS) was a more delayed response to UV‐B than to drought. H 2 O 2 was detected during both stresses, whereas · OH radical production was a more characteristic response to drought. The present characterization of transgenic tobacco plants revealed a common role for aldose/aldehyde reductase (ALR) in the detoxification of lipid peroxidation products under water depletion and UV‐B irradiation. As the result of the increased synthesis of ALR enzyme, the transformed plants were more tolerant to both stress conditions, exhibiting reduced loss of photosynthetic function and decreased accumulation of TBARS and H 2 O 2 as compared to control (SR1) plants. When plants had been exposed to mild, non‐lethal drought and were then watered again to recover, they were more tolerant to a subsequent stress by UV‐B. This was characteristic to both transgenic and wild‐type plants. However, this drought‐induced cross‐tolerance to UV‐B stress of SR1 tobacco did not reach the enhancement achieved by the overexpression of ALR.