Involvement of mitochondrial pathway in benzo[a]pyrene-induced neuron apoptosis:

摘要: Benzo[a]pyrene (B[a]P), a well-known carcinogen, is widespread in the environment. Although neurotoxic effect of B[a]P has not drawn much attention, toxic effects on learning and memory have been reported. Since it well known that neuronal apoptosis plays major role impairment triggered by many stimuli, an effort made to examine whether B[a]P-induced neurotoxicity occurs through mitochondria-mediated apoptosis. Cultured newborn rat cerebral neurons were used clarify induced study. After incubating with different doses presence S9 for 40 h, apoptotic rates B[a]P-treated increased dose-dependent manner. Further analysis showed was accompanied loss mitochondrial membrane potential, release cytochrome c from mitochondria cytosol, downregulation antiapoptotic protein B-cell lymphoma-2 (Bcl-2) levels concurrent upregulation proapoptotic Bcl-2-associated X (Bax) levels, increase activities caspases-9 -3. However, there no difference activity caspase-8 between B[a]P-exposed controls. Collectively, these results upregulates Bax downregulates Bcl-2 expression cultured neurons, which leads c, caspase-3 activation death.