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[目的]观察高摄铝状态下燃煤型氟中毒大鼠肝脏超微结构的变化。[方法]将断乳2周的SD纯系大鼠24只(雌雄各半)按体质量随机分为3组,每组8只,即对照组、高氟组、高氟铝组。对照组食用非病区玉米加工的饲料(含氟5.20mg/L,含铝6.80mg/L),饮用普通自来水(含氟0.69mg/L,含铝0.20mg/L)。其余两组则食用以病区玉米为主加工而成的饲料(含氟110.00mg/kg,含铝19.70mg/L),高氟铝组还饮用自来水配制的高铝水(含氟0.70mg/L,含铝90.00mg/L)。实验期为22周。处死前收集大鼠24h尿液用于测定尿氟、铝的水平,处死后取大鼠四肢骨用于测定骨氟,取大鼠肝脏用于在透射电镜下观察肝脏的超微结构变化。[结果](1)骨氟:高氟铝组[(204.07±63.78)mg/kg]、高氟组[(199.90±106.84)mg/kg]的骨氟高于对照组[(30.06±6.11)mg/kg],组间比较差异均有统计学意义(t=0.62、0.53,P﹤0.01)。(2)尿氟:高氟铝组、高氟组的尿氟[(4.52±3.09)、(5.50±0.74)mg/L]均高于对照组[(0.89±0.36)],t=0.23、0.55,P均﹤0.05)。(3)骨铝:对照组的骨铝水平[(3.32±3.02)mg/kg]明显低于高氟铝组[(374.21±56.11)mg/kg]。(4)尿铝:高氟铝组的尿铝水平[(1.14±0.32)mg/L]高于对照组[(0.73±0.11)mg/L],t=1.92,P均﹤0.05]。(5)肝脏的超微结构:高氟组大鼠肝细胞细胞核轻度皱缩、凹陷,异染色质凝聚,边集,少数线粒体空泡化,线粒体嵴消失,内质网轻度扩张;高氟铝组大鼠肝细胞核轻度皱缩、凹陷,形似土豆,细胞内粗面内质网轻度扩张,部分线粒体周围有间隙,线粒体基质电子密度增大,线粒体嵴模糊不清,部分细胞内可见纤维化。[结论]建立了高摄铝状态下燃煤型氟中毒大鼠模型;高氟能引起肝损害,高氟和高铝对肝脏的损伤有协同作用的趋势。
[Objective] To observe the changes of liver ultrastructure in coal-fired fluorosis rats exposed to high photoluminescence. [Method] Twenty-four SD male rats were randomly divided into three groups according to body weight, with 8 rats in each group, namely control group, high fluoride group and high fluorine aluminum group. The control group consumed non-watertown maize processed feed (containing 5.20mg / L of fluoride and 6.80mg / L of aluminum), drinking ordinary tap water (0.69mg / L of fluorine and 0.20mg / L of aluminum). The remaining two groups were fed with feed mainly made of maize (containing 110.00mg / kg of fluorine and 19.70mg / L of aluminum), high aluminum fluoride drinking water (0.70mg / L, Aluminum 90.00 mg / L). The experiment period is 22 weeks. 24 h urinary excretion of rats was collected before sacrifice for the determination of urinary fluoride and aluminum levels. After the rats were sacrificed, the limb extremities were taken for the determination of bone fluoride, and the liver of the rats was taken for observing the ultrastructural changes of the liver under transmission electron microscope. [Results] (1) Bone Fluoride was significantly higher in the high fluoride group [(204.07 ± 63.78) mg / kg] and high fluoride group (199.90 ± 106.84 mg / kg) than in the control group [(30.06 ± 6.11) mg / kg]. The difference between the two groups was statistically significant (t = 0.62, 0.53, P <0.01). (2) Urinary fluoride: Urinary fluoride in high fluoride group and high fluoride group were significantly higher than those in control group [(4.52 ± 3.09), (5.50 ± 0.74) mg / L, respectively, 0.23 ± 0.36, 0.55, P <0.05). (3) Bone-aluminum: The level of bone aluminum in the control group [(3.32 ± 3.02) mg / kg] was significantly lower than that in the group with high fluoride-aluminum [(374.21 ± 56.11) mg / kg] (4) Urinary aluminum: The level of urinary aluminum in high fluoride group [(1.14 ± 0.32) mg / L] was higher than that in the control group [(0.73 ± 0.11) mg / L], t = 1.92, P <0.05; (5) The ultrastructure of liver: The liver cells of high fluoride group had mild shrinkage of nucleus, condensed and heterochromatin aggregation, marginal set, few mitochondria vacuolization, disappearance of mitochondrial cristae and mild endoplasmic reticulum expansion; Fluoroaluminum group rats liver cell nucleus mild shrinkage, depression, like potatoes, intracellular rough endoplasmic reticulum mild expansion, some mitochondria around the gap, the mitochondrial matrix electron density increased mitochondrial cristae blurred, part of the intracellular Visible fibrosis. [Conclusion] A rat model of coal-induced fluorosis was established under high photoluminescence. High fluoride could cause liver damage, and high fluoride and high aluminum had a synergistic effect on liver injury.