Programmed cell death is not mediated by a p53 homolog in Pisum sativum

2000 ◽  
Vol 56 (5) ◽  
pp. 197-206 ◽  
Author(s):  
S.J. Klosterman ◽  
J.J. Choi ◽  
L.A. Hadwiger
Keyword(s):  
Cell Death ◽  
Pisum Sativum ◽  
Programmed Cell Death

scholarly journals Structural Evidence of Programmed Cell Death Induction by Tungsten in Root Tip Cells of Pisum sativum

Plants ◽  
2019 ◽  
Vol 8 (3) ◽  
pp. 62 ◽  
Author(s):  
Ioannis-Dimosthenis Adamakis ◽  
Eleftherios Eleftheriou
Keyword(s):  
Cell Death ◽  
Pisum Sativum ◽  
Programmed Cell Death ◽  
Laser Scanning ◽  
Laser Scanning Microscopy ◽  
Root Tip ◽  
Confocal Laser ◽  
Golgi Bodies ◽  
Tip Cells ◽  
Root Tip Cells

Previous studies have shown that excess tungsten (W), a rare heavy metal, is toxic to plant cells and may induce a kind of programmed cell death (PCD). In the present study we used transmission electron microscopy (TEM) and confocal laser scanning microscopy (CLSM) to investigate the subcellular malformations caused by W, supplied as 200 mg/L sodium tungstate (Na2WO4) for 12 or 24 h, in root tip cells of Pisum sativum (pea), The objective was to provide additional evidence in support of the notion of PCD induction and the presumed involvement of reactive oxygen species (ROS). It is shown ultrastructurally that W inhibited seedling growth, deranged root tip morphology, induced the collapse and deformation of vacuoles, degraded Golgi bodies, increased the incidence of multivesicular and multilamellar bodies, and caused the detachment of the plasma membrane from the cell walls. Plastids and mitochondria were also affected. By TEM, the endoplasmic reticulum appeared in aggregations of straight, curved or concentric cisternae, frequently enclosing cytoplasmic organelles, while by CLSM it appeared in bright ring-like aggregations and was severely disrupted in mitotic cells. However, no evidence of ROS increase was obtained. Overall, these findings support the view of a W-induced vacuolar destructive PCD without ROS enhancement.

Programmed Cell Death Ligand 1 and Venous Thromboembolism in Patients with Primary Brain Tumors

2019 ◽  
Author(s):  
P. Seyed Mir ◽  
A.-S. Berghoff ◽  
M. Preusser ◽  
G. Ricken ◽  
J. Riedl ◽  
...  
Keyword(s):  
Cell Death ◽  
Venous Thromboembolism ◽  
Programmed Cell Death ◽  
Brain Tumors ◽  
Primary Brain Tumors

Glial cytotoxicity of low doses of cadmium as a model of heavy metal pollution influence on vertebrates

2020 ◽  
Vol 31 (1) ◽  
pp. 3-10
Author(s):  
V. S. Nedzvetsky ◽  
V. Ya. Gasso ◽  
A. M. Hahut ◽  
I. A. Hasso
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Oxidative Damage ◽  
Cadmium Chloride ◽  
Glioma Cells ◽  
Low Doses ◽  
Genotoxic Effects ◽  
Cadmium Ions

Cadmium is a common transition metal that entails an extremely wide range of toxic effects in humans and animals. The cytotoxicity of cadmium ions and its compounds is due to various genotoxic effects, including both DNA damage and chromosomal aberrations. Some bone diseases, kidney and digestive system diseases are determined as pathologies that are closely associated with cadmium intoxication. In addition, cadmium is included in the list of carcinogens because of its ability to initiate the development of tumors of several forms of cancer under conditions of chronic or acute intoxication. Despite many studies of the effects of cadmium in animal models and cohorts of patients, in which cadmium effects has occurred, its molecular mechanisms of action are not fully understood. The genotoxic effects of cadmium and the induction of programmed cell death have attracted the attention of researchers in the last decade. In recent years, the results obtained for in vivo and in vitro experimental models have shown extremely high cytotoxicity of sublethal concentrations of cadmium and its compounds in various tissues. One of the most studied causes of cadmium cytotoxicity is the development of oxidative stress and associated oxidative damage to macromolecules of lipids, proteins and nucleic acids. Brain cells are most sensitive to oxidative damage and can be a critical target of cadmium cytotoxicity. Thus, oxidative damage caused by cadmium can initiate genotoxicity, programmed cell death and inhibit their viability in the human and animal brains. To test our hypothesis, cadmium cytotoxicity was assessed in vivo in U251 glioma cells through viability determinants and markers of oxidative stress and apoptosis. The result of the cell viability analysis showed the dose-dependent action of cadmium chloride in glioma cells, as well as the generation of oxidative stress (p <0.05). Calculated for 48 hours of exposure, the LD50 was 3.1 μg×ml-1. The rates of apoptotic death of glioma cells also progressively increased depending on the dose of cadmium ions. A high correlation between cadmium concentration and apoptotic response (p <0.01) was found for cells exposed to 3–4 μg×ml-1 cadmium chloride. Moreover, a significant correlation was found between oxidative stress (lipid peroxidation) and induction of apoptosis. The results indicate a strong relationship between the generation of oxidative damage by macromolecules and the initiation of programmed cell death in glial cells under conditions of low doses of cadmium chloride. The presented results show that cadmium ions can induce oxidative damage in brain cells and inhibit their viability through the induction of programmed death. Such effects of cadmium intoxication can be considered as a model of the impact of heavy metal pollution on vertebrates.

Dynamical analysis of the programmed cell death pathway

2007 ◽  
Author(s):  
Luciano Carotenuto ◽  
Vincenza Pace ◽  
Dina Bellizzi ◽  
Giovanna De Benedictis
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Dynamical Analysis ◽  
Cell Death Pathway

Biological response of the organism to the introduction of metal nanocomposites

2020 ◽  
pp. 761-762
Author(s):  
L. M. Sosedova ◽  
V. S. Rukavishnikov ◽  
E. A. Titov
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Biological Response ◽  
Brain Cell ◽  
Metal Nanocomposites ◽  
The Brain

The results of a study on rats toxicity of nanoparticles of metals bismuth, gadolinium and silver encapsulated in a natural biopolymer matrix arabinogalactan are presented. When intake of nanocomposite of silver revealed the readiness of the brain cell to apoptosis. The effect of bismuth and gadolinium nanocomposites did not cause an increase in the process of programmed cell death.

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