RESUMEN
OBJECTIVE: To investigate the expression of caspase-3, Bcl-2, and Bax in pentavalent vanadium-induced neuronal apoptosis and the neurotoxicity of pentavalent vanadium to in vitro cultured rat neurons. METHODS: Neurons from rats were cultured in vitro and treated with different concentrations of V2O5. Neuronal apoptosis was evaluated by TdT-mediated dUTP-biotin nick end labeling (TUNEL). The expression of caspase-3, Bcl-2, and Bax in neurons was measured by Western blot. The images collected by gel imaging system and scanner were analyzed. RESULTS: The TUNEL showed that compared with the control group, the middle- and high-dose exposure groups had significantly increased apoptosis index (AI) of neurons (P < 0.05 or P < 0.01). The Western blot showed that compared with the control group, the middle- and high-dose exposure groups had significantly increased expression of caspase-3 and Bax and significantly decreased expression of Bcl-2 (P <0.05 or P < 0.01). The AI of neurons was positively correlated with the expression of caspase-3 and Bax (r = 0.943, P < 0.01; r = 0.937, P < 0.01) and negatively correlated with the expression of Bcl-2 (r = -0.908, P < 0.01). CONCLUSION: Pentavalent vanadium may induce neuronal apoptosis, and the expression of caspase-3, Bcl-2, and Bax, which regulate apoptosis, plays an important role in the neuronal apoptosis induced by pentavalent vanadium.