The modulation of the toxic effects of 2AA on the liver by apoptosis was investigated. The arylamine 2-aminoanthracene (2AA) is an aromatic hydrocarbon employed in manufacturing chemicals, dyes, inks, and as curing agents in epoxy resins and polyurethanes. 2AA has been detected in tobacco smoke and cooked foods. Analysis of total mRNA extracts from liver for apoptosis-related gene expression changes was coupled with liver tissue histology (H&E staining), TUNEL and Caspase-3 activity assays. Specific apoptosis staining showed greater level of apoptosis in medium- and high-dose 2AA treated animals. Apoptosis does not seem to occur directly via caspase-3 activation mechanism. Analyses of apoptosis-related genes seem to show AEN and BAX as the main targets in the induction of apoptosis in response to 2AA exposure. Dose-dependent increases in mRNA expression were observed in all genes except caspase 3. Bax was highly expressed in the high-dose rats belonging to the 2-week exposure group.
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