ArticlePlanta2010
Nitric oxide modulates cadmium influx during cadmium-induced programmed cell death in tobacco BY-2 cells.
Article in Planta, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
33 citing papers in PubMed, 144 citations in OpenAlex.
- Cadmium Toxicity inFoods (Basel, Switzerland) · 2025Article
- Influencing Factors ofToxics · 2023Article
- The Core Jasmonic Acid-Signalling ModuleCurrent issues in molecular biology · 2022Article
- The Role of Nitric Oxide Signaling in Plant Responses to Cadmium Stress.International journal of molecular sciences · 2022Review
- Melatonin Protects Tobacco Suspension Cells against Pb-Induced Mitochondrial Dysfunction.International journal of molecular sciences · 2021Article
- Cryopreserved-pollen viability is regulated by NO-induced programmed cell death.Plant cell reports · 2021Article
- The involvement of gaseous signaling molecules in plant MAPK cascades: function and signal transduction.Planta · 2021Review
- Melatonin alleviates cadmium toxicity by reducing nitric oxide accumulation and IRT1 expression in Chinese cabbage seedlings.Environmental science and pollution research international · 2021Article
- Review
- Hydrogen sulfide negatively regulates cd-induced cell death in cucumber (Cucumis sativus L) root tip cells.BMC plant biology · 2020Article
- The ROS-associated programmed cell death causes the decline of pollen viability recovered from cryopreservation in Paeonia lactiflora.Plant cell reports · 2020Article
- NO and ABA Interaction Regulates Tuber Dormancy and Sprouting in Potato.Frontiers in plant science · 2020Article
- Nitric Oxide Enhances Cytotoxicity of Lead by Modulating the Generation of Reactive Oxygen Species and Is Involved in the Regulation of PbPlants (Basel, Switzerland) · 2019Article
- Current approaches to measure nitric oxide in plants.Journal of experimental botany · 2019Review
- Cadmium and Plant Development: An Agony from Seed to Seed.International journal of molecular sciences · 2019Review
- Protein S-nitrosylation in programmed cell death in plants.Cellular and molecular life sciences : CMLS · 2019Review
- Expression of the Tobacco Non-symbiotic Class 1 Hemoglobin Gene Hb1 Reduces Cadmium Levels by Modulating Cd Transporter Expression Through Decreasing Nitric Oxide and ROS Level inFrontiers in plant science · 2019Article
- Toxic effects of cadmium on tall fescue and different responses of the photosynthetic activities in the photosystem electron donor and acceptor sides.Scientific reports · 2017Article
- Computational Analysis on Down-Regulated Images of Macrophage Scavenger Receptor.Pharmaceutical research · 2017Article
- Exogenous GR24 Alleviates Cadmium Toxicity by Reducing Cadmium Uptake in Switchgrass (Panicum virgatum) Seedlings.International journal of environmental research and public health · 2017Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nitric oxide (NO) is a bioactive gas and functions as a signaling molecule in plants exposed to diverse biotic and abiotic stresses including cadmium (Cd(2+)). Cd(2+) is a non-essential and toxic heavy metal, which has been reported to induce programmed cell death (PCD) in plants. Here, we investigated the role of NO in Cd(2+)-induced PCD in tobacco BY-2 cells (Nicotiana tabacum L. cv. Bright Yellow 2). In this work, BY-2 cells exposed to 150 microM CdCl(2) underwent PCD with TUNEL-positive nuclei, significant chromatin condensation and the increasing expression of a PCD-related gene Hsr203J. Accompanied with the occurring of PCD, the production of NO increased significantly. The supplement of NO by sodium nitroprusside (SNP) had accelerated the PCD, whereas the NO synthase inhibitor Nomega-nitro-L-arginine methyl ester hydrochloride (L-NAME) and NO-specific scavenger 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO) alleviated this toxicity. To investigate the mechanism by which NO exerted its function, Cd(2+) concentration was measured subsequently. SNP led more Cd(2+) content than Cd(2+) treatment alone. By contrast, the prevention of NO by L-NAME decreased Cd(2+) accumulation. Using the scanning ion-selective electrode technique, we analyzed the pattern and rate of Cd(2+) fluxes. This analysis revealed the promotion of Cd(2+) influxes into cells by application of SNP, while L-NAME and cPTIO reduced the rate of Cd(2+) uptake or even resulted in net Cd(2+) efflux. Based on these founding, we concluded that NO played a positive role in CdCl(2)-induced PCD by modulating Cd(2+) uptake and thus promoting Cd(2+) accumulation in BY-2 cells.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.