Abstract:
[Objective] To observe the effects of subchronic benzo[a]pyrene (B[a]P) exposure on cell apoptosis in hippocampus of rats, to analyze its correlation with the impairment of learning and memory, and to explore the mechanism of B[a]P neurotoxicity.
[Methods] According to the results of Morris water maze test, 48 healthy adult male SD rats were divided into 6 groups:1 blank control, 1 olive control and 4 B[a]P groups (with 0.5, 1.5, 4.5 and 10.0 mg/kg bw ip injection for 90 days respectively). The learning and memory function was tested by Morris water maze. Cell apoptosis in hippocampus of rats was detected by flow cytometry.
[Results] The Morris water maze test results showed that the 4.5 and 10.0mg/kg B[a]P groups' average escape latencies were significantly higher than blank control group's, olive control group's, 0.5 and 1.5 mg/kg B[a]P groups' (P < 0.05). The 10.0 mg/kg B[a]P group's frequency of crossing platform and swimming time percentage in platform quadrant were significantly lower than blank control group's, olive control group's, and 0.5 and 1.5 mg/kg B[a]P groups' (P < 0.05). The 4.5 mg/kg B[a]P group's fr equency of crossing platform and swimming time percentage in platform quadrant were significantly lower than blank control group's, olive control group's, and 0.5 mg/kg B[a]P group's (P < 0.05). The 10.0 mg/kg B[a]P group's swimming time in platform quadrant was significantly lower than blank control group's, olive control group's, and 0.5 mg/kg B[a]P group's (P < 0.05). The 10.0 mg/kg B[a]P group's early and total hippocampal apoptosis rates were significantly higher than the rest groups'(P < 0.05). Pearson correlation analysis showed that there were positive correlations between early apoptosis rate and average escape latencies (r=0.542, P < 0.05). The early hippocampal apoptosis rate was negatively correlated with and the swimming time in platform quadrant (r=-0.395, P<0.05), and the swimming time percentage in platform quadrant (r=-0.592, P < 0.05).
[Conclusion] Subchronic exposure to B[a]P leads to cell apoptosis in hippocampus of rats and damage of learning and memory. The results suggest that hippocampal apoptosis in rats may be a possible mechanism to result in learning and memory impairment.