We found a match
Your institution may have access to this item. Find your institution then sign in to continue.
- Title
AlCl<sub>3</sub> causes Fas/Fas-L mediated cell death in the cortex and hippocampus of mouse brain.
- Authors
Keshava, Rohini; Vazhayil, Vikas; Mitra, Rohan; Bhagavatula, Indira Devi; Gope, Rajalakshmi
- Abstract
In this study effect of sustained toxicity of low dose of aluminum trichloride (AlCl3, Anhydrous) in mouse brain and liver was evaluated. Six weeks old Swiss albino mice were given orally 2 mg AlCl3/ kg body weight / per day for three consecutive weeks. Three weeks after last feeding the brain and liver tissues were examined for histopathological changes which revealed Al toxicity related changes. Oral administration AlCl3 caused a slight decrease in the whole-body weight and a significant decrease in the weight of liver and brain tissues. In addition, AlCl3 ingestion resulted in increased level of total protein in the liver but decreased the same in the brain tissue in the experimental mice. AlCl3 feeding also caused DNA laddering that is characteristics of apoptotic cell death in the liver and brain tissues. Moreover, AlCl3 feeding lead to decreased level of anti-apoptotic Bcl2 and PI3K proteins, and increased levels of p53 as well as pro-apoptotic phospho c-Jun N-terminal kinase (pJNK), Bax, Caspase 3, p21 and Fas proteins in the cortex and in the hippocampus regions. Trace level of Fas protein was present in the cortex and hippocampus regions of the control brain which increased to 2 to 3-fold upon AlCl3 feeding. Higher level of Fas ligand was present in the cortex and hippocampus regions of the control and it remained unchanged with AlCl3 ingestion. Our data shows that the observed cell death caused by AlCl3 in the cortex and hippocampus region of mouse brain could be Fas mediated.
- Subjects
HIPPOCAMPUS (Brain); CELL death; FAS proteins; BRAIN death; ALUMINUM chloride
- Publication
International Journal of BioSciences & Technology, 2019, Vol 12, Issue 3, p21
- ISSN
0974-3987
- Publication type
Article
- DOI
10.5281/zenodo.3369193