论文部分内容阅读
[目的]观察苯并(a)芘[B(a)P]在大鼠海马中的分布及对其神经元的损害。[方法]将150只SD大鼠随机分为对照组和实验组,实验组尾静脉注射14C-B(a)P 3.7×105 Bq/kg,对照组注射相同剂量的生理盐水。在染毒后1、6、12、24、48 h,用光镜自显影法观察14C-B(a)P在大鼠脑组织中的分布,HE染色光镜和电镜观察14C-B(a)P对大鼠海马CA1区神经元的损害。[结果]光镜放射自显影观察表明,在海马组织中的14C-B(a)P银粒数随染毒后时间的延长而逐渐增加,24 h达到高峰,48 h明显减少,1、6、12、24、48 h银粒数分别为(22.31±2.11)、(23.11±2.32)、(25.97±2.97)、(28.16±3.17)、(17.16±1.85)粒/mm3,差异具有统计学意义(F=28.65,P<0.01)。HE染色光镜观察发现:染毒后12 h海马神经元细胞排列稀疏、数量减少,核变小、部分出现固缩现象,随着时间的推移,损害逐渐加重。电镜观察发现:大鼠海马神经元及细胞器在染毒后不同时间点有不同程度的损害,主要表现为海马神经纤维水肿,脱髓鞘样改变、线粒体肿胀、高尔基复合体扩张、核膜部分溶解,突触前膜致密斑明显。[结论]14C-B(a)P在海马组织中的分布随时间的增加而增加,24 h达到高峰;不同时间点B(a)P对海马神经元有不同程度的损害。
[Objective] To observe the distribution of benzo (a) pyrene [B (a) P] in rat hippocampus and its damage to neurons. [Method] 150 SD rats were randomly divided into control group and experimental group. The experimental group received intravenous injection of 14C-B (a) P 3.7 × 105 Bq / kg and the control group received the same dose of saline. At 1, 6, 12, 24 and 48 hours after exposure, the distribution of 14C-B (a) P in rat brain was observed by light microscopy. HE staining and electron microscopy were used to observe the distribution of 14C-B ) P on Neurons in Hippocampal CA1 Area of Rats. [Result] The autoradiography of light microscope showed that the number of silver grains of 14C-B (a) P in hippocampus gradually increased with the prolongation of exposure time, reached its peak at 24 hours and decreased significantly at 48 hours. (22.31 ± 2.11), (23.11 ± 2.32), (25.97 ± 2.97), (28.16 ± 3.17) and (17.16 ± 1.85) g / mm3 at 12, 24 and 48 h, respectively, the difference was statistically significant (F = 28.65, P <0.01). The results of HE staining showed that the neurons in the hippocampus were sparsely arranged and their numbers decreased, the nuclei became smaller, and the phenomenon of condensation was observed in some of the neurons at 12 h after exposure. As time went on, the damage gradually increased. Electron microscopy showed that hippocampal neurons and organelles had different degrees of damage at different time points after exposure, mainly including changes of hippocampal nerve fiber edema, demyelination, swelling of mitochondria, dilation of Golgi complex, partial dissolution of nuclear membrane , The presynaptic membrane dense spot obvious. [Conclusion] The distribution of 14C-B (a) P in hippocampus increased with time and peaked at 24 h. B (a) P had different degrees of damage to hippocampal neurons at different time points.