Search claims · PlantClaims

Intervention effectobservedoriginal resultmeasured

Claim · model-written summary

The proteasome inhibitor MG132 suppressed H2O2-induced PCD in BY-2 cells.

Taxon: tobacco Bright Yellow-2 (BY-2) cellse0
Treatment: proteasome inhibitor MG132e4
Outcome: H2O2-induced PCDe4
Direction: suppressede4

Not reportedComparator

Verbatim

e0
“H2O2-induced programmed cell death (PCD) of tobacco Bright Yellow-2 (BY-2) cells”
✓ located verbatim in the source · abstract, characters 0–80

e4
“The proteasome inhibitor MG132 suppressed the H2O2-induced PCD”
✓ located verbatim in the source · abstract, characters 864–926

Title

Inactivation of Carbonyl-Detoxifying Enzymes by H2O2 Is a Trigger to Increase Carbonyl Load for Initiating Programmed Cell Death in Plants

Md. Sanaullah Biswas; Ryota Terada; Jun’ichi Mano Antioxidants 2020. doi:10.3390/antiox9020141

Other claims from this paper (7)

Intervention effectobservedoriginal resultpositivemeasured

Claim · model-written summary

JL54 induced rapid H2O2 accumulation, lignin deposition and localized programmed cell death in Larix.

Taxon: Larix olgensisLarix gmelinii var. olgensise1
Treatment: JL54e0
Outcome: hydrogen peroxide (H2O2) accumulation, extensive lignin deposition, and localized programmed cell death (PCD)e0
Direction: accumulatione0

Not reportedComparator

Verbatim

e0
“JL54-induced rapid hydrogen peroxide (H2O2) accumulation, extensive lignin deposition, and localized programmed cell death (PCD)”
✓ located verbatim in the source · abstract, characters 611–739

e1
“Larix olgensis”
✓ located verbatim in the source · abstract, characters 0–14

Title

Integrative Transcriptomic and Biochemical Profiling Reveals Bacillus amyloliquefaciens JL54 Primes Larix olgensis Defenses Against Neofusicoccum laricinum Attack

Xiangyu Zhao; Fengze Yang; Lingyu Kong; et al. Plants 2026. doi:10.3390/plants15081181

Other claims from this paper (8)

Intervention effect JL54 pretreatment reduced shoot blight disease incidence in Larix by 12.5%.
Intervention effect JL54 pretreatment achieved 43.75% shoot blight control efficacy in Larix.
Intervention effect JL54 pretreatment maintained Larix host vigor.
Observation At 0 h post-inoculation, Larix defense showed upregulation of cutin, suberin and wax biosynthesis pathways.
Observation At 12 h post-inoculation, Larix responses were dominated by ribosome and proteostasis related pathways.
Intervention effect JL54 colonization reduced Larix malondialdehyde content by 27.2%.
Intervention effect JL54 colonization significantly increased POD, PAL and GST defense enzyme activities in Larix.
Mechanism Phytohormone profiling implicated JA signaling as central to JL54-induced systemic resistance and preceding pathogen containment.

Intervention effectobservedoriginal resultnegativemeasured

Claim · model-written summary

Hydrogen peroxide induced programmed cell death in tobacco Bright Yellow-2 cultures.

Taxon: tobaccoNicotiana tabacume0
Material: Bright Yellow-2 (TBY-2)e0
Treatment: 50 mM H₂O₂e0
Outcome: PCDe0

Not reportedComparatorDirection

Verbatim

e0
“The addition of 50 mM H₂O₂ to tobacco Bright Yellow-2 (TBY-2) cell cultures induces PCD.”
✓ located verbatim in the source · abstract, characters 191–279

Title

The soluble proteome of tobacco Bright Yellow-2 cells undergoing H2O2-induced programmed cell death

C. Vannini; M. Marsoni; C. Cantara; et al. Journal of Experimental Botany 2012. doi:10.1093/jxb/ers031

Other claims from this paper (8)

Intervention effectobservedoriginal resultnegativemeasured

Claim · model-written summary

Hydrogen peroxide at 5 mM induced programmed cell death.

Taxon: soybeanGlycine maxt0
Treatment: Hydrogen peroxide (5 mM)e0
Outcome: PCDe0

Not reportedComparatorDirection

Verbatim

e0
“Hydrogen peroxide (5 mM) induced PCD.”
✓ located verbatim in the source · abstract, characters 140–177

t0
“soybean suspension cell cultures”
✓ located verbatim in the source · title, characters 90–122

Title

Involvement of the mitochondrial KATP+ channel in H2O2- or NO-induced programmed death of soybean suspension cell cultures

V. Casolo Journal of Experimental Botany 2005. doi:10.1093/jxb/eri093

Other claims from this paper (16)

Intervention effect Cells treated with 20 mM H2O2 became necrotic, with intermediate necrapoptotic hallmarks before that.
Observation ATP and glucose-6-phosphate stayed constant during programmed cell death.
Observation ATP and glucose-6-phosphate decreased significantly in necrotic cells.
Intervention effect Succinate-dependent oxygen consumption was slightly uncoupled in mitochondria from 5 mM H2O2-treated cells.
Intervention effect Mitochondrial electrical potential difference weakly decreased after 5 mM H2O2 treatment.
Intervention effect KCl caused greater partial dissipation of delta psi in treated mitochondria than in controls.
Mechanism CsA induced delta psi formation in de-energized mitochondria through K+ efflux.
Intervention effect CsA-induced K+ efflux was reduced in mitochondria from treated cells.
Observation Mitochondria from 1 mM sodium nitroprusside-treated cells showed the same response pattern and apoptotic symptoms.
Intervention effect Succinate-dependent oxygen consumption was completely uncoupled in necrotic cells treated with 20 mM H2O2.
Intervention effect Delta psi generation was significantly inhibited in necrotic cells treated with 20 mM H2O2.
Intervention effect CsA-dependent delta psi formation was prevented in necrotic cells treated with 20 mM H2O2.
Intervention effect Mitochondrial swelling was partly prevented in apoptotic cells compared with control cells.
Intervention effect Mitochondrial swelling was completely prevented in necrotic cells compared with control cells.
Observation Moderate swelling accompanied slight outer-membrane rupture and cytochrome c release.
Mechanism The authors implicate a K(+)ATP channel in H2O2- or NO-induced programmed cell death.

Intervention effectobservedoriginal resultmeasured

Claim · model-written summary

Decreasing intracellular polyamines in samdc downregulating plants enhanced salinity-induced PCD.

Taxon: tobaccoNicotiana tabacume0
Material: samdc downregulating transgenic plantse5
Treatment: decreasing intracellular PAse5
Outcome: salinity-induced PCDe5
Direction: enhancede5

Not reportedComparator

Verbatim

e0
“we developed a series of tobacco (Nicotiana tabacum cv Xanthi) transgenic plants overexpressing or downregulating apoplastic polyamine oxidase (PAO; S-pao and A-pao plants, respectively) or downregulating S-adenosyl-l-methionine decarboxylase (samdc plants)”
✓ located verbatim in the source · abstract, characters 234–491

e5
“decreasing intracellular PAs, while keeping normal apoplastic Spd oxidation, as in samdc downregulating transgenic plants, caused enhanced salinity-induced PCD”
✓ located verbatim in the source · abstract, characters 1153–1312

Title

Spermidine Exodus and Oxidation in the Apoplast Induced by Abiotic Stress Is Responsible for H2O2 Signatures That Direct Tolerance Responses in Tobacco

Panagiotis N. Moschou; Konstantinos A. Paschalidis; Ioannis D. Delis; et al. The Plant Cell 2008. doi:10.1105/tpc.108.059733

Other claims from this paper (9)

Intervention effect A-pao tobacco plants accumulated less H2O2 than wild-type plants under salt stress.
Intervention effect A-pao tobacco plants showed less programmed cell death than wild-type plants under salt stress.
Intervention effect S-pao tobacco plants had higher H2O2 levels under salt stress.
Intervention effect S-pao tobacco plants failed to accumulate stress-responsive mRNAs under salt stress.
Intervention effect Stress-responsive genes were efficiently induced in wild-type and A-pao plants, at a lower rate in A-pao plants.
Observation Tobacco plants secreted spermidine into the apoplast under salt stress.
Mechanism Apoplastic spermidine oxidized by the apoplastic PAO generates H2O2.
Association Induction of stress-responsive genes or PCD depended on the level of spermidine-derived apoplastic H2O2.
Mechanism Accumulated H2O2 induces tolerance responses or PCD, depending also on intracellular polyamine levels.

Intervention effectobservedoriginal resultmeasured

Claim · model-written summary

Cobalt delayed GA-induced programmed cell death in wheat aleurone layers.

Taxon: wheatTriticum aestivume0
Organ / stage: aleurone layerse0
Treatment: cobalte0
Outcome: programmed cell death (PCD)e0
Direction: delaye0

Not reportedComparator

Verbatim

e0
“cobalt is able to delay gibberellic acid (GA)-induced programmed cell death (PCD) in wheat aleurone layers”
✓ located verbatim in the source · abstract, characters 171–277

Title

Cobalt Alleviates GA-Induced Programmed Cell Death in Wheat Aleurone Layers via the Regulation of H2O2 Production and Heme Oxygenase-1 Expression

Mingzhu Wu; Jiale Li; Fangquan Wang; et al. International Journal of Molecular Sciences 2014. doi:10.3390/ijms151121155

Other claims from this paper (9)

Intervention effect Carbon monoxide pretreatment produced a similar delay of cell death.
Intervention effect Bilirubin pretreatment produced a similar delay of cell death.
Mechanism Increased HO-1 expression contributed to cobalt alleviation of cell death.
Intervention effect ZnPPIX substantially prevented cobalt-induced increases in HO-1 activity.
Intervention effect ZnPPIX substantially prevented cobalt-induced alleviation of cell death.
Mechanism Cobalt-induced initial H2O2 production may stimulate HO-1 expression.
Mechanism Cobalt-induced initial H2O2 production may alleviate cell death.
Observation Cobalt-induced SOD, CAT and APX expression and activities were consistent with H2O2 accumulation during GA treatment.
Intervention effect ZnPPIX differentially blocked cobalt responses.

Intervention effectobservedoriginal resultmeasured

Claim · model-written summary

ZnPPIX substantially prevented cobalt-induced alleviation of cell death.

Taxon: WheatTriticum aestivumt0
Treatment: zinc protoporphyrin-IX (ZnPPIX)e0
Outcome: alleviation of PCDe0
Direction: preventede0

Not reportedComparator

Verbatim

e0
“The application of HO-1-specific inhibitor, zinc protoporphyrin-IX (ZnPPIX), substantially prevented the increases of HO-1 activity and the alleviation of PCD triggered by cobalt.”
✓ located verbatim in the source · abstract, characters 526–705

t0
“Wheat”
✓ located verbatim in the source · title, characters 54–59

Title

Cobalt Alleviates GA-Induced Programmed Cell Death in Wheat Aleurone Layers via the Regulation of H2O2 Production and Heme Oxygenase-1 Expression

Mingzhu Wu; Jiale Li; Fangquan Wang; et al. International Journal of Molecular Sciences 2014. doi:10.3390/ijms151121155

Other claims from this paper (9)

Intervention effect Cobalt delayed GA-induced programmed cell death in wheat aleurone layers.
Intervention effect Carbon monoxide pretreatment produced a similar delay of cell death.
Intervention effect Bilirubin pretreatment produced a similar delay of cell death.
Mechanism Increased HO-1 expression contributed to cobalt alleviation of cell death.
Intervention effect ZnPPIX substantially prevented cobalt-induced increases in HO-1 activity.
Mechanism Cobalt-induced initial H2O2 production may stimulate HO-1 expression.
Mechanism Cobalt-induced initial H2O2 production may alleviate cell death.
Observation Cobalt-induced SOD, CAT and APX expression and activities were consistent with H2O2 accumulation during GA treatment.
Intervention effect ZnPPIX differentially blocked cobalt responses.

Intervention effectobservedoriginal resultmeasured

Claim · model-written summary

H2O2 added to cell-free protein extract inactivated the carbonyl reductase.

Taxon: tobacco Bright Yellow-2 (BY-2) cellse0
Treatment: The addition of H2O2 to cell-free protein extracte6
Gene: carbonyl reductasee6
Outcome: carbonyl reductasee6
Direction: inactivatede6

Not reportedComparator

Verbatim

e0
“H2O2-induced programmed cell death (PCD) of tobacco Bright Yellow-2 (BY-2) cells”
✓ located verbatim in the source · abstract, characters 0–80

e6
“The addition of H2O2 to cell-free protein extract inactivated the carbonyl reductase”
✓ located verbatim in the source · abstract, characters 1027–1111

Title

Inactivation of Carbonyl-Detoxifying Enzymes by H2O2 Is a Trigger to Increase Carbonyl Load for Initiating Programmed Cell Death in Plants

Md. Sanaullah Biswas; Ryota Terada; Jun’ichi Mano Antioxidants 2020. doi:10.3390/antiox9020141

Other claims from this paper (7)

Intervention effectobservedoriginal resultnegativemeasured

Claim · model-written summary

Both heat shock and peroxide induced increased S-nitrosylating agents during programmed cell death.

Taxon: tobaccoNicotiana tabacume0
Treatment: heat shock (HS) or hydrogen peroxide (H2O2)e0
Outcome: S-nitrosylating agentse0
Direction: increasee0

Not reportedComparator

Verbatim

e0
“during programmed cell death (PCD), induced by both heat shock (HS) or hydrogen peroxide (H2O2) in tobacco (Nicotiana tabacum) Bright Yellow-2 cells, an increase in S-nitrosylating agents occurred”
✓ located verbatim in the source · abstract, characters 314–510

Title

S-Nitrosylation of Ascorbate Peroxidase Is Part of Programmed Cell Death Signaling in Tobacco Bright Yellow-2 Cells

M. C. de Pinto; V. Locato; A. Sgobba; et al. PLANT PHYSIOLOGY 2013. doi:10.1104/pp.113.222703

Other claims from this paper (7)

Intervention effect NO increased during both induced cell deaths, less under peroxide than heat shock.
Intervention effect GSNO increased in peroxide-treated cells.
Intervention effect GSNO decreased after heat shock.
Observation GSNO reductase activity and expression were low after peroxide and high after heat shock.
Intervention effect Both stimuli induced S-nitrosylated proteins.
Observation cAPX was S-nitrosylated at the onset of both cell deaths.
Mechanism S-nitrosylation of cAPX caused a rapid decrease in its activity.

Intervention effectobservedoriginal resultnegativemeasured

Claim · model-written summary

Early SQ-1 treatment increased reactive oxygen species production in wheat leaves.

Taxon: wheatTriticum aestivume0
Organ / stage: leavese0
Treatment: CHA-SQ-1e0
Outcome: production of reactive oxygen species (O2 and H2O2)e0
Direction: excesse0

Not reportedComparator

Verbatim

t0
“wheat”
✓ located verbatim in the source · title, characters 68–73

e0
“CHA-SQ-1 trig-gered organelle changes and PCD in wheat leaves accompanied by excess production of reactive oxygen species (O2 and H2O2)”
✓ located verbatim in the source · abstract, characters 579–714

Title

Programmed cell death, antioxidant response and oxidative stress in wheat flag leaves induced by chemical hybridization agent SQ-1

Shu-ping WANG; Gai-sheng ZHANG; Qi-lu SONG; et al. Journal of Integrative Agriculture 2016. doi:10.1016/s2095-3119(14)60977-1

Other claims from this paper (10)

Intervention effect Chemical hybridization agent induced programmed cell death in wheat flag leaves.
Intervention effect Early SQ-1 treatment caused organelle changes in wheat leaves.
Intervention effect Early SQ-1 treatment induced programmed cell death in wheat leaves.
Intervention effect Early SQ-1 treatment down regulated superoxide dismutase, catalase and guaiacol peroxidase activities.
Mechanism SQ-1 treatment produced ladder like wheat leaf DNA patterns, indicating endonuclease activation.
Intervention effect SQ-1 treatment strongly activated lipid peroxidation in wheat leaves.
Intervention effect SQ-1 treatment inhibited photosynthesis in wheat leaves.
Observation Chemical hybridization agent content in wheat leaves declined over time after application.
Observation Young wheat flag leaves regained oxidative and antioxidative balance.
Observation Young wheat flag leaves developed into mature green leaves.

“H2O2-induced PCD”

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