Publication Date:
2012-04-15
Description:
Population surveys and animal experiments have shown that rare earth elements (REEs) cause neurological defects. However, the detailed mechanisms underlying these effects are still unclear. Given that lanthanum is commonly used for investigating into REEs-induced neurological defects, this study chose lanthanum chloride (LaCl 3 ) to show that LaCl 3 promotes mitochondrial apoptotic pathway in primary cultured rat astrocytes by regulating expression of Bcl-2 family proteins. The main findings of this study are (1) LaCl 3 treatment (0.25, 0.5, and 1.0 mM for 12–48 h) induced the astrocytes damages with a concentration-dependent manner, which were confirmed with methyl thiazolyl tetrazolium and lactate dehydrogenase release assays, and morphological examination. (2) A 24 h treatment of LaCl 3 concentration-dependently decreased mitochondrial membrane potential, increased cytochrome c release from mitochondria into cytosol, elevated caspase 9 and 3 expression, and promoted astrocyte apoptosis. (3) LaCl 3 treatment increased the ratio of pro-apoptotic Bax and antiapoptotic Bcl-2 proteins, which in turn broke the balance among pro-apoptotic and antiapoptotic Bcl-2 family proteins, leading to astrocyte apoptosis. Our results indicate that LaCl 3 alters Bcl-2 family protein expressions, which in turn promote mitochondrial apoptotic pathway, and thus astrocytic damage. © 2011 Wiley Periodicals, Inc. Environ Toxicol, 2011.
Print ISSN:
1520-4081
Electronic ISSN:
1522-7278
Topics:
Energy, Environment Protection, Nuclear Power Engineering
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