Claim · model-written summary
ROS production in PCD cells was accompanied by early inhibition of glucose oxidation
- Taxon
- tobacco (Nicotiana tabacum)
Nicotiana tabacume0 - Compound
- ROSe1
- Outcome
- glucose (Glc) oxidatione1
- Direction
- inhibitione1
Not reportedMaterialGeneOrgan / stageInteractorInteractor roleSecond interactorSecond interactor roleTreatmentComparatorSettingValueQualifier
Organisms pictured · Representative pictures of the matched species, not figures from the paper.
Verbatim
e0“tobacco (Nicotiana tabacum) Bright-Yellow 2 cells”
e1“Production of ROS in PCD cells was accompanied by early inhibition of glucose (Glc) oxidation”
Title
Rosa Anna Vacca; Maria Concetta de Pinto; Daniela Valenti; et al. PLANT PHYSIOLOGY 2004. doi:10.1104/pp.103.035956
Other claims from this paper (13)
- Intervention effect Heat treatment at 55 degrees C triggered programmed cell death in tobacco BY-2 cells, complete after 72 h
- Observation Cells undergoing PCD showed an immediate burst of hydrogen peroxide and superoxide anion production in the early phase
- Intervention effect Cell death was prevented by the antioxidant ascorbate (ASC)
- Intervention effect Cell death was prevented by superoxide dismutase (SOD)
- Intervention effect Actinomycin D prevented cell death with a lower efficiency
- Intervention effect Cycloheximide prevented cell death with a lower efficiency
- Observation Induction of PCD resulted in gradual oxidation of endogenous ascorbate
- Association PCD was accompanied by a decrease in the amount and specific activity of cytosolic ascorbate peroxidase
- Observation A reduction in cAPX gene expression was found in the late PCD phase
- Observation Changes in cAPX kinetic properties were found in PCD cells
- Observation PCD cells showed a strong impairment of mitochondrial function, shown by an increase in cellular NAD(P)H fluorescence
- Observation Mitochondria isolated from PCD cells failed to generate membrane potential and to oxidize succinate
- Mechanism ROS production in early PCD may occur because of damage to the cell antioxidant system, with impairment of mitochondrial oxidative phosphorylation