OBJECTIVETo 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.

METHODSNeurons 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.

RESULTSThe 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).

CONCLUSIONPentavalent 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.