Heavy metal-induced reactive oxygen species and cell death in barley root tip

2017 ◽  
Vol 140 ◽  
pp. 34-40 ◽  
Author(s):  
Ladislav Tamás ◽  
Igor Mistrík ◽  
Veronika Zelinová
Keyword(s):  
Reactive Oxygen Species ◽  
Heavy Metal ◽  
Cell Death ◽  
Reactive Oxygen ◽  
Barley Root ◽  
Root Tip ◽  
Oxygen Species ◽  
Barley Root Tip

Role of reactive oxygen species-generating enzymes and hydrogen peroxide during cadmium, mercury and osmotic stresses in barley root tip

Planta ◽  
2009 ◽  
Vol 231 (2) ◽  
pp. 221-231 ◽  
Author(s):  
Ladislav Tamás ◽  
Igor Mistrík ◽  
Jana Huttová ◽  
L’ubica Halušková ◽  
Katarína Valentovičová ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Hydrogen Peroxide ◽  
Reactive Oxygen ◽  
Barley Root ◽  
Root Tip ◽  
Oxygen Species ◽  
Barley Root Tip

scholarly journals Nitric Oxide Enhances Cytotoxicity of Lead by Modulating the Generation of Reactive Oxygen Species and Is Involved in the Regulation of Pb2+ and Ca2+ Fluxes in Tobacco BY-2 Cells

Plants ◽  
2019 ◽  
Vol 8 (10) ◽  
pp. 403 ◽  
Author(s):  
Jiaye Wu ◽  
Yue Zhang ◽  
Ruizhi Hao ◽  
Yuan Cao ◽  
Xiaoyi Shan ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Heavy Metal ◽  
Cell Death ◽  
Calcium Homeostasis ◽  
Reactive Oxygen ◽  
Ros Generation ◽  
Plant Responses ◽  
Oxygen Species ◽  
In Cells

Lead is a heavy metal known to be toxic to both animals and plants. Nitric oxide (NO) was reported to participate in plant responses to different heavy metal stresses. In this study, we analyzed the function of exogenous and endogenous NO in Pb-induced toxicity in tobacco BY-2 cells, focusing on the role of NO in the generation of reactive oxygen species (ROS) as well as Pb2+ and Ca2+ fluxes using non-invasive micro-test technology (NMT). Pb treatment induced BY-2 cell death and rapid NO and ROS generation, while NO burst occurred earlier than ROS accumulation. The elimination of NO by 2-4-carboxyphenyl-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO) resulted in a decrease of ROS, and the supplementation of NO by sodium nitroprusside (SNP) caused an increased accumulation of ROS. Furthermore, the addition of exogenous NO stimulated Pb2+ influx, thus promoting Pb uptake in cells and aggravating Pb-induced toxicity in cells, whereas the removal of endogenous NO produced the opposite effect. Moreover, we also found that both exogenous and endogenous NO enhanced Pb-induced Ca2+ effluxes and calcium homeostasis disorder. These results suggest that exogenous and endogenous NO played a critical regulatory role in BY-2 cell death induced by Pb stress by promoting Pb2+ influx and accumulation and disturbing calcium homeostasis.

scholarly journals Transcriptome profiling of kenaf (Hibiscus cannabinus L.) under plumbic stress conditions implies the involvement of NAC transcription factors regulating reactive oxygen species-dependent programmed cell death

PeerJ ◽  
2020 ◽  
Vol 8 ◽  
pp. e8733
Author(s):  
Xia An ◽  
Jie Chen ◽  
Guanrong Jin
Keyword(s):  
Reactive Oxygen Species ◽  
Heavy Metal ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Molecular Mechanisms ◽  
De Novo ◽  
Reactive Oxygen ◽  
Hibiscus Cannabinus ◽  
Differentially Expressed ◽  
Oxygen Species

Heavy metal contamination of soils has become a serious global issue, and bioremediation has been proposed as a potential solution. Kenaf (Hibiscus cannabinus L.) is a fast growing, non-woody multipurpose annual plant that is suitable for removing excess heavy metals from soils. However, there has been relatively little research on the kenaf molecular mechanisms induced in response to an exposure to heavy metal stress. Thus, whole kenaf seedlings grown under control (normal) and stress (plumbic treatment) conditions were sampled for transcriptome sequencing. Unigenes generated through the de novo assembly of clean reads were functionally annotated based on seven databases. Transcription factor (TF)-coding genes were predicted and the physiological traits of the seedlings were analyzed. A total of 44.57 Gb high-quality sequencing data were obtained, which were assembled into 136,854 unigenes. These unigenes included 1,697 that were regarded as differentially expressed genes (DEGs). A GO enrichment analysis of the DEGs indicated that many of them are related to catalytic activities. Moreover, the DEGs appeared to suggest that numerous KEGG pathways are suppressed (e.g., the photosynthesis-involving pathways) or enhanced (like the flavonoid metabolism pathways) in response to Pb stress. Of the 2,066 predicted TF-coding genes, only 55 were differentially expressed between the control and stressed samples. Further analyses suggested that the plumbic stress treatment induced reactive oxygen species-dependent programmed cell death in the kenaf plants via a process that may be regulated by the differentially expressed NAC TF genes.

scholarly journals 4-Hydroxychalcone Induces Cell Death via Oxidative Stress in MYCN-Amplified Human Neuroblastoma Cells

2019 ◽  
Vol 2019 ◽  
pp. 1-16 ◽  
Author(s):  
Amnah M. Alshangiti ◽  
Eszter Tuboly ◽  
Shane V. Hegarty ◽  
Cathal M. McCarthy ◽  
Aideen M. Sullivan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Cell Death ◽  
Cytotoxic Effect ◽  
Neuroblastoma Cells ◽  
Reactive Oxygen ◽  
Prognostic Indicator ◽  
Oxygen Species ◽  
Human Neuroblastoma Cells ◽  
Human Neuroblastoma

Neuroblastoma is an embryonal malignancy that arises from cells of sympathoadrenal lineage during the development of the nervous system. It is the most common pediatric extracranial solid tumor and is responsible for 15% of childhood deaths from cancer. Fifty percent of cases are diagnosed as high-risk metastatic disease with a low overall 5-year survival rate. More than half of patients experience disease recurrence that can be refractory to treatment. Amplification of the MYCN gene is an important prognostic indicator that is associated with rapid disease progression and a poor prognosis, highlighting the need for new therapeutic approaches. In recent years, there has been an increasing focus on identifying anticancer properties of naturally occurring chalcones, which are secondary metabolites with variable phenolic structures. Here, we report that 4-hydroxychalcone is a potent cytotoxin for MYCN-amplified IMR-32 and SK-N-BE (2) neuroblastoma cells, when compared to non-MYCN-amplified SH-SY5Y neuroblastoma cells and to the non-neuroblastoma human embryonic kidney cell line, HEK293t. Moreover, 4-hydroxychalcone treatment significantly decreased cellular levels of the antioxidant glutathione and increased cellular reactive oxygen species. In addition, 4-hydroxychalcone treatment led to impairments in mitochondrial respiratory function, compared to controls. In support of this, the cytotoxic effect of 4-hydroxychalcone was prevented by co-treatment with either the antioxidant N-acetyl-L-cysteine, a pharmacological inhibitor of oxidative stress-induced cell death (IM-54) or the mitochondrial reactive oxygen species scavenger, Mito-TEMPO. When combined with the anticancer drugs cisplatin or doxorubicin, 4-hydroxychalcone led to greater reductions in cell viability than was induced by either anti-cancer agent alone. In summary, this study identifies a cytotoxic effect of 4-hydroxychalcone in MYCN-amplified human neuroblastoma cells, which rationalizes its further study in the development of new therapies for pediatric neuroblastoma.

scholarly journals CBIO-07. CELL DEATH INDUCED BY AN OSCILLATING MAGNETIC FIELD IN PATIENT DERIVED GLIOBLASTOMA CELLS IS MEDIATED BY REACTIVE OXYGEN SPECIES

2020 ◽  
Vol 22 (Supplement_2) ◽  
pp. ii17-ii17
Author(s):  
Shashank Hambarde ◽  
Martyn Sharpe ◽  
David Baskin ◽  
Santosh Helekar
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Cell Viability ◽  
Cortical Neurons ◽  
Reactive Oxygen ◽  
Great Promise ◽  
Antioxidant Vitamin ◽  
Ros Generation ◽  
Oxygen Species ◽  
Novel Therapy

Abstract Noninvasive cancer therapy with minimal side effects would be ideal for improving patient outcome in the clinic. We have developed a novel therapy using strong rotating magnets mounted on a helmet. They generate oscillating magnetic fields (OMF) that penetrate through the skull and cover the entire brain. We have demonstrated that OMF can effectively kill patient derived glioblastoma (GBM) cells in cell culture without having cytotoxic effects on cortical neurons and normal human astrocytes (NHA). Exposure of GBM cells to OMF reduced the cell viability by 33% in comparison to sham-treated cells (p< 0.001), while not affecting NHA cell viability. Time lapse video-microscopy for 16 h after OMF exposure showed a marked elevation of mitochondrial reactive oxygen species (ROS), and rapid apoptosis of GBM cells due to activation of caspase 3. Addition of a potent antioxidant vitamin E analog Trolox effectively blocked OMF-induced GBM cell death. Furthermore, OMF significantly potentiated the cytotoxic effect of the pro-oxidant Benzylamine. The results of our studies demonstrate that OMF-induced cell death is mediated by ROS generation. These results demonstrate a potent oncolytic effect on GBM cells that is novel and unrelated to any previously described therapy, including a very different mechanism of action and different technology compared to Optune therapy. The effect is very powerful, and unlike Optune, can be seen within hours after initiation of treatment. We believe that this technology holds great promise for new, effective and nontoxic treatment of glioblastoma.

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