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Chilling‐induced Ca 2+ overload enhances production of active oxygen species in maize ( Zea mays L.) cultured cells: the effect of abscisic acid treatment
Author(s) -
Chen W. P.,
Li P. H.
Publication year - 2001
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.1365-3040.2001.00729.x
Subject(s) - lipid peroxidation , abscisic acid , egta , reactive oxygen species , extracellular , calcium , superoxide , chemistry , biochemistry , plant physiology , oxidative stress , biophysics , biology , botany , enzyme , organic chemistry , gene
Chilling (4 °C) induced a prolonged high level of intracellular Ca 2+ (Ca 2+ overload) and lipid peroxidation in maize ( Zea mays L. cv Black Mexican Sweet) cultured cells. However, such Ca 2+ overload and enhanced lipid peroxidation were not seen in abscisic acid (ABA)‐treated cells, which had an improved chilling tolerance. A Ca 2+ ionophore, A23187, caused Ca 2+ overload in both ABA‐treated maize cells and the untreated control, whereas an enhanced lipid peroxidation was detected only in the control. The high level of active oxygen species (AOS) in the control during chilling at 4 °C could be reduced by the presence of lanthanum (La 3+ ), a Ca 2+ channel blocker, in the medium. Moreover, both the A23187‐induced lipid peroxidation and AOS production in the control could be reduced by extracellular EGTA, a Ca 2+ chelator. Laser‐scanning confocal microscopy revealed that mitochondria were one of the major AOS sources under chilling and during A23187 treatment. In vitro assays showed that superoxide production in isolated maize mitochondria was enhanced by the presence of Ca 2+ . Findings suggest that chilling‐induced Ca 2+ influx in the control triggers a marked generation of AOS, which in turn results in the enhanced lipid peroxidation. The ability of ABA‐treated cells to avoid the chilling‐induced Ca 2+ influx may serve as a mechanism that prevents the chilling‐induced oxidative stress and thus results in less chilling injury.