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亚急性氟暴露家兔每日摄入80mg/kp氟化钠(自由饮用1000ppm氟化钠水溶液)1个月,慢性氟暴露家兔每日摄入20mg/kg氟化钠4个月或6个月。肾脏酶学研究结果表明,慢性氟暴露使尿r-谷氨酰转肽酶(r-GT)排出量增加。该影响出现较早、持续时间较长,但有逐渐减弱的趋势。氟还可使肾碱性磷酸酶(AKP)、肾琥珀酸脱氢酶(SDH)、肾酸性磷酸酶(AcP)活性降低,有一定的剂量和时间依赖性。上述细胞器标志酶活性的改变,提示肾小管上皮细胞刷状缘、线粒体和溶酶体的功能已受损。 在亚急性实验期间同时给予80mg/kg氟化钠和120mg/kg四硼酸钠,慢性实验期间同时给予20mg/kg氟化钠和30mg/kg四硼酸钠,硼可减轻氟对尿r-GT和肾AKP、肾SDH、肾AcP活性的影响,表明硼对氟性肾功能损伤具有一定的抵抗作用。
Subacute fluoride exposure in rabbits daily intake of 80mg / kp sodium fluoride (free drinking 1000ppm sodium fluoride solution) 1 month, chronic fluoride exposure rabbit daily intake of 20mg / kg of sodium fluoride for 4 months or 6 month. Renal enzymology results show that chronic fluoride exposure increases urinary glutamyl transpeptidase (r-GT) excretion. The impact appeared earlier, longer duration, but gradually weakened trend. Fluorine can also reduce renal alkaline phosphatase (AKP), renal succinate dehydrogenase (SDH), renal acid phosphatase (AcP) activity, with a certain dose and time-dependent. Changes in the organelle-labeled enzyme activity suggest that the functions of the brush border, mitochondria and lysosomes of renal tubular epithelial cells have been impaired. 80 mg / kg sodium fluoride and 120 mg / kg sodium tetraborate were given concurrently during the subacute test and 20 mg / kg sodium fluoride and 30 mg / kg sodium tetraborate were given concurrently during the chronic phase. Boron reduced fluoride exposure to urinary r-GT and Kidney AKP, renal SDH, renal AcP activity, indicating that boron has a certain resistance to renal damage of fluorine.