2024-03-28T23:36:32Zhttp://digital.csic.es/dspace-oai/requestoai:digital.csic.es:10261/893332022-06-01T12:29:58Zcom_10261_105com_10261_1col_10261_358
Cell viability and proteomic analysis in cultured neurons exposed to methylmercury
Vendrell, Iolanda
Carrascal, Montserrat
Vilaró, Maria Teresa
Rodríguez-Farré, Eduard
Suñol, Cristina
Glutamate transport
Cell proteome
Lipid peroxidation
Neurotoxicity
Primary cultures
Cerebellar granule cells
Methylmercury is an environmental contaminant with special selectivity for cerebellar granule cells. The aim of this study was to determine the effect of long-term methylmercury exposure on cell viability and cellular proteome in cultured cerebellar granule cells. Primary cultures of mice cerebellar granule cells were treated with 0-300 nM methylmercury at 2 days in vitro (div) and afterwards the cells were harvested at 12 div. 100 nM methylmercury produced loss of cell viability, reduced intracellular glutamate content and increased lipid peroxidation. Glutamate transport was not modified by methylmercury treatment. Cell death induced by 300 nM methylmercury at 8 div was apoptotic without producing activation of caspase 3. Extracts of total protein were separated by 2D electrophoresis. Around 800 protein spots were visualized by silver staining in SDS-polyacrylamide gels. Gel images were digitized and protein patterns were analysed by image analysis. Several spots were identified through a combination of peptide mass fingerprinting and matrix-assisted laser desorption/ionization-time of flight-mass spectrometry (MALDI-TOF-MS). The mitochondrial protein 3-ketoacid-coenzyme A transferase I was decreased up to 39% of controls at concentrations of methylmercury that did not produce cytotoxic effects, whereas the cytoplasmic proteins lactate dehydrogenase chain B and actin did not change.
2014-01-13T12:45:50Z
2014-01-13T12:45:50Z
2007
2014-01-13T12:45:50Z
artículo
Human and Experimental Toxicology 26(4): 263-272 (2007)
http://hdl.handle.net/10261/89333
10.1177/0960327106070455
eng
closedAccess
Sage Publications