• Corpus ID: 14014796

Low Dose and Long Term Toxicity of Sodium Arsenite Caused Caspase Dependent Apoptosis Based on Morphology and Biochemical Character

  title={Low Dose and Long Term Toxicity of Sodium Arsenite Caused Caspase Dependent Apoptosis Based on Morphology and Biochemical Character},
  author={Mohammad Hussein Abnosi and Zahra Jafari Yazdi},
  journal={Cell Journal (Yakhteh)},
  pages={161 - 170}
Objective: Although arsenite is toxic it is currently recommended for the treatment of malignancies. In this study the effects of sub-micromolar concentrations of sodium arsenite on the viability, morphology and mechanism of cell death of rat bone marrow mesenchymal stem cells (BMCs) over 21 days was investigated. Materials and Methods: In this experimental study, BMCs were extracted in Dulbecco’s Modified Eagles Medium (DMEM) containing 15% of fetal bovine serum (FBS) and expanded till the 3rd… 

Figures and Tables from this paper

Programmed Cell Death of Cultured A549 Lung Epithelial Cells Induced by Sodium Arsenite Exposure
It is demonstrated that exposure to NaAsO2 in vitro can lead to cell death and at low concentration NaAs O2 can induce autophagy and at high concentration it can induce apoptosis.
Biochemical and morphological changes in bone marrow mesenchymal stem cells induced by treatment of rats with p-Nonylphenol
It was revealed that the p-NP treatment of rats caused significant reduction in nuclear diameter, cytoplasm shrinkage, and induction of caspase-dependent-apoptosis following osteogenic differentiation.
The viability and mineralization of cells treated with SA reduced significantly and the calcium and alkalinphosphatase activity of the cells decreased significantly with 1 and 25 nM concentrations of SA when compared with control.
Inhibition of Kupffer cell functions modulates arsenic intoxication in Wistar rats.
The inhibition of Kupffer cell functions by GdCl3 suppressed arsenic intoxication improving the liver function indices, oxidative stress status, lipid profile, neutrophilic inflammation and ultimately restored the cellular architecture.
In-vitro hematological toxicity prediction by colony-forming cell assays
Applications, limitations and future prospective of in vitro tests for hematotoxicity with emphasis on the techniques involved in the Colony forming unit culture systems are described.
Nuclear translocation of nuclear factor kappa B is regulated by G protein signaling pathway in arsenite‐induced apoptosis in HBE cell line
It is demonstrated for the first time that arsenite‐induced nuclear translocation of nuclear factor kappa B (NF‐κB) resulted in the release of cytochrome c, the modulation of Fas and FasL, caspase activation, and ultimately leading to cell apoptosis, which suggests that inhibition of G protein‐mediated pathway by specific inhibitors may be a potential strategy for the prevention of arsenite toxicity.
Alternative methods in toxicology: CFU assays application, limitation and future prospective
A critical view over in vitro hematopoietic colony-forming cell assays in assessment of hematotoxicity is provided.
Morphine Preconditioning Downregulates MicroRNA-134 Expression Against Oxygen-Glucose Deprivation Injuries in Cultured Neurons of Mice
The neuronal cell survival rate was significantly higher, and the amount of apoptotic neurons was significantly decreased in neurons preconditioned with morphine before OGD than that of OGD alone.


Butylhydroquinone protects cells genetically deficient in glutathione biosynthesis from arsenite-induced apoptosis without significantly changing their prooxidant status.
  • S. Kann, C. Estes, A. Puga
  • Biology
    Toxicological sciences : an official journal of the Society of Toxicology
  • 2005
Results suggest that regulation of glutathione levels by GCLM determines the sensitivity to arsenic-induced apoptosis by setting the overall ability of the cells to mount an effective antioxidant response.
Mechanisms involved in sodium arsenite‐induced apoptosis of human neutrophils
It is demonstrated that arsenite induces PMN apoptosis through an oxygen‐dependent mechanism that can be prevented through selective antioxidants and the antioxidants catalase, dimethyl sulfoxide, DMSO, glutathione, GSH, NAC, and taurine were significantly protective against arsenite‐induced apoptosis.
Study on the toxic effects induced by different arsenicals in primary cultured rat astroglia.
Early induction of genetic instability and apoptosis by arsenic in cultured Chinese hamster cells.
Arsenic induced early genetic instability or apoptosis in dividing cells, and while apoptosis tended to cease when arsenic was removed from the culture medium, the acquired instability remained and propagated within the cell population.
Arsenite Delays Progression through Each Cell Cycle Phase and Induces Apoptosis following G2/M Arrest in U937 Myeloid Leukemia Cells
An overall reduction in cell cycle progression rather than induction of arrest at one specific checkpoint is found and arsenic's ability to inhibit growth in any cell cycle phase may increase its value as a chemotherapeutic used together with other, more phase-selective agents, such as camptothecin.
Differential effect of sodium arsenite during the activation of human CD4+ and CD8+ T lymphocytes.
Lysosomes and trivalent arsenic treatment in acute promyelocytic leukemia.
In APL cells, arsenite may cause rapid destabilization of lysosomes, and the mechanism of arsenite-induced PML/RAR alpha degradation was investigated, which was inhibited by protease inhibitors.