Polychlorinated biphenyl mixtures (Aroclors) induce apoptosis via Bcl-2, Bax and caspase-3 proteins in neuronal cell cultures.

Polychlorinated biphenyls (PCBs) are a group of persistent and widely dispersed environmental pollutants, some of which may be neurotoxic. In the present study, we have investigated the effect of PCB commercial mixtures (Aroclors) on neuronal cell cultures by assessing cell viability and apoptotic cell death. We have combined morphological and biochemical techniques to establish the relevance of apoptosis in neuronal cell death induced by Aroclors. Treatment with both Aroclor 1248 and Aroclor 1260 caused the loss of cell viability and accelerated apoptosis both in a concentration- and time-dependent manner. However, the extent of apoptosis resulted greater for Aroclor 1248 than for Aroclor 1260. This is correlated with the loss of cell viability since Aroclor 1248 is more cytotoxic. The apoptosis induced by Aroclors involves the increase of caspase-3 activity. To correlate the caspase-3 activity with respect to changes in protein processing, caspase-3 precursor protein (procaspase-3) was evaluated by Western blot analysis. Also, Bcl-2 and Bax protein were assessed in order to elucidate the cell death machinery induced in cortical neuronal cell cultures by Aroclor 1248. The results indicate that the increase in Aroclor-induced apoptosis correlates with a reduction in the expression of antiapoptotic Bcl-2 and an increase in the expression of proapoptotic Bax. These results suggest that, with our experimental conditions, Aroclors induce apoptosis in primary cultures of cortical neurons via proteins of the Bcl-2 and caspase families.