Claim · model-written summary
Chilling induced prolonged intracellular calcium overload in maize cells.
- Material
- Black Mexican Sweete0
- Organ / stage
- cultured cellse0
- Treatment
- Chilling (4 °C)e0
- Outcome
- intracellular Ca 2+ (Ca 2+ overload)e0
- Direction
- inducede0
Not reportedGeneCompoundInteractorInteractor roleSecond interactorSecond interactor roleComparatorSettingValueQualifier
Organisms pictured · Representative pictures of the matched species, not figures from the paper.

Verbatim
e0“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.”
Title
W. P. Chen; P. H. Li Plant Cell & Environment 2001. doi:10.1046/j.1365-3040.2001.00729.x
Other claims from this paper (10)
- Intervention effect Chilling induced lipid peroxidation in maize cells.
- Intervention effect ABA-treated cells avoided chilling-induced calcium overload and enhanced lipid peroxidation and had improved chilling tolerance.
- Intervention effect A23187 caused calcium overload in both ABA-treated and untreated maize cells.
- Intervention effect A23187 enhanced lipid peroxidation only in untreated control maize cells.
- Intervention effect Lanthanum reduced active oxygen species in chilling maize control cells.
- Intervention effect Extracellular EGTA reduced A23187-induced lipid peroxidation in control cells.
- Intervention effect Extracellular EGTA reduced A23187-induced active oxygen species production.
- Observation Mitochondria were a major source of active oxygen species during chilling and A23187 treatment.
- Intervention effect Calcium enhanced superoxide production in isolated maize mitochondria.
- Mechanism The authors infer that chilling-induced calcium influx triggers active oxygen species generation and lipid peroxidation.