Objective To observe the effects of subchronic benzoapyrene (BaP) 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 BaP 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 BaP 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 BaP groups' average escape latencies were significantly higher than blank control group's, olive control group's, 0.5 and 1.5 mg/kg BaP groups' (P < 0.05). The 10.0 mg/kg BaP 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 BaP groups' (P < 0.05). The 4.5 mg/kg BaP 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 BaP group's (P < 0.05). The 10.0 mg/kg BaP group's swimming time in platform quadrant was significantly lower than blank control group's, olive control group's, and 0.5 mg/kg BaP group's (P < 0.05). The 10.0 mg/kg BaP 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 BaP 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.
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