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目的复制燃煤型氟中毒大鼠模型并观察其对海马CA1区形态学影响。方法 24只SD大鼠随机分为3组,对照组、低、高氟组;染氟组以地氟病区燃煤烘烤的玉米为主要饲料,复制氟中毒动物模型,6个月后用氟离子选择电极法检测动物尿、骨及脑氟含量,观察大鼠海马CA1区神经元病理变化,用Biomias 2000图象分析系统测试大鼠海马CA1区神经元胞体平均面积、周长及平均灰度值。结果低、高氟组大鼠尿氟为(2.87±0.12)、(5.27±0.15)mg/L,骨氟(2 912±140)、(4 624±20)mg/kg,脑氟(1.14±0.04)、(1.79±0.04)mg/kg;与对照组尿氟(1.68±0.02)mg/L、骨氟(1479±127)mg/kg、脑氟(0.52±0.05)mg/kg比较,差异有统计学意义(P<0.05或P<0.01);尼氏染色显示,与对照组大鼠神经元平均灰度值(115±4)比较,染氟组大鼠均明显增加[低氟(157±7),高氟(164±8)]。结论长期食用燃煤型氟中毒病区燃煤烘烤的粮食可以引起氟中毒;并导致动物尿、骨、脑氟含量增高,使大鼠海马CA1区神经元蛋白合成功能下降。
OBJECTIVE: To duplicate the rat model of fluorosis caused by coal combustion and observe its effect on the morphology of hippocampal CA1 area. Methods Twenty-four SD rats were randomly divided into three groups: control group, low and high fluoride groups. In the fluorine-exposed group, Fluoride ion-selective electrode method was used to detect urinary, bone and brain fluoride contents in hippocampal CA1 neurons in rats. Biomias 2000 image analysis system was used to measure the average area, perimeter and average gray Degree value. Results The urinary fluoride in low and high fluoride groups were (2.87 ± 0.12), (5.27 ± 0.15) mg / L, 2 912 ± 140, (4624 ± 20) mg / kg and 1.14 ± 0.04, 1.79 ± 0.04 mg / kg, respectively. Compared with the control group, urinary fluoride (1.68 ± 0.02) mg / L, (P <0.05 or P <0.01). Compared with the control group, the average gray value of neurons in the control group (115 ± 4) was significantly increased (P <0.05 or P <0.01) ± 7), high fluoride (164 ± 8)]. Conclusions Food poisoning caused by long-term burning of coal-fired fluorosis areas can cause fluorosis. And lead to increased urinary, bone and brain fluoride levels in rats and decrease the neuronal protein synthesis in hippocampal CA1 area of rats.