Assessment of Caenorhabditis Elegans Germline Cell Cycle Arrest and Apoptosis for Heavy Metals Toxicity Testing

Author(s):  
Shunchang Wang ◽  
Xun Luo ◽  
Lijun Wu
2007 ◽  
Vol 20 (2) ◽  
pp. 181-186 ◽  
Author(s):  
Shunchang Wang ◽  
Ye Zhao ◽  
Lijun Wu ◽  
Mingli Tang ◽  
Caixing Su ◽  
...  

Drug Research ◽  
2020 ◽  
Vol 70 (12) ◽  
pp. 545-551 ◽  
Author(s):  
Sara Mirjalili ◽  
Maedeh Dejamfekr ◽  
Abdolvahab Moshtaghian ◽  
Mehdi Salehi ◽  
Mahdi Behzad ◽  
...  

AbstractCompounds containing heavy metals such as vanadium, nickel, and cobalt may be useful for the treatment of various diseases. Multiple studies have been carried out on the anticancer effects of vanadium-contained compounds on different cell types. This study aimed to evaluate the role of schiff base oxovanadium complex ([N,N'-bis(3-methoxy-salicylidene)-1,2-phenylenediamine]Vanadium(IV) Oxide Complex) on cell cycle arrest and different cell cycle phases in MKN45 cell of gastric cancer. Schiff base oxovanadium complex was used to assessthe amount of cytotoxicity via cell viability test. PI color and flow cytometry technique were applied to evaluate the effects of vanadium synthetic compounds on cell cycle phases; subsequently, we analyzed the change rates of gene expression in P53, GADD45, and CDC25 genes, which are involved in cell division phases. The findings indicated that the vital activities of time-dependent and concentration-dependent MKN45 cells with schiff base oxovanadium complex were significantly reduced; therefore, this complex is able to inhibit the migration of cancer cells and metastatic activities in a time-dependent mode. Cell cycle arrest was obtained after 48 h of treatment in phase G2/M at 1 microgram/milliliter (μg/ml) concentration. This is probably attributed to the increased gene expression of P53 and GADD45 genes and reduced gene expression of CDC25 gene. Compounds containing such heavy metals as vanadium decrease the growth, proliferation, and migration of MKN45 cells. They arrest cell cycle in phase G2/M via changing the controllers of cell division phases activated due to DNA damage.


2009 ◽  
Vol 390 (1) ◽  
Author(s):  
Eva Ondroušková ◽  
Jana Slováčková ◽  
Vendula Pelková ◽  
Jiřina Procházková ◽  
Karel Souček ◽  
...  

Abstract The Bcl-2 protein is one of the key components of biochemical pathways controlling programmed cell death. The function of this protein can be regulated by posttranslational modifications. Phosphorylation of Bcl-2 has been considered to be significantly associated with cell cycle arrest in the G2/M phase of the cell cycle, and with cell death caused by defects of microtubule dynamics. This study shows that phosphorylation of Bcl-2 can be induced by heavy metals due to activation of the Jun N-terminal kinase pathway that is not linked to the G2/M cell cycle arrest. Furthermore, we demonstrate that hyperphosphorylated Bcl-2 protein is a more potent inhibitor of zinc-induced cell death than its hypophosphorylated mutant form. These data suggest that regulation of Bcl-2 protein function by phosphorylation is an important part of cell responses to stress.


2005 ◽  
Vol 43 (05) ◽  
Author(s):  
M Gerhard ◽  
C Schmees ◽  
R Rad ◽  
P Voland ◽  
T Treptau ◽  
...  

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