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硼抗氟性肾组织损伤的超微结构研究 被引量:17

Ultrastructural study on anti-damage effects of Boron on kidney during subacute and chronic exposure to fluoride
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摘要 亚急性氟暴露家兔每日摄入80mg/kg 氟化钠一个月,慢性氟暴露家兔每日摄入20mg/kg 氟化钠四或六个月。肾脏病理学研究结果表明氟暴露剂量和时间与肾小管病变程度和性质呈一定的剂量——效应和时间——效应关系。肾小管管腔中高度浓缩的氟可能是主要的、直接的致病原因。肾脏超微结构研究发现,慢性氟暴露时肾小管上皮细胞內多种细胞器均有损伤。主要表现为线粒体肿胀变性、内质网广泛扩张、微绒毛轻度脱失、基底反褶消失、粗面内质网脱粒、核蛋白体解聚、大量自噬性溶酶体形成以及肾间质增生性改变。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,硼可减轻氟对肾组织细胞乃至亚细胞结构的损伤。 Rabbits subacutely exposed to fluoride accepted daily 80 mg/kg sodiumfluoride in drinking water during an one-month period,and the otherschronically exposed to fluoride accepted daily 20 mg/kg sodium fluoride indrinking water during a four or six-month period.The result of thepathological study revealed that there was a relation of dose-effect or time-effectbetween the dose or duration of fluoride exposure and the extent or character ofdamage of fluoride to renal tubules.It was considered that the fluoride highlyconcentrated in renal tubules was the chief and direct cause responsible for thedamage to renal tubular cells.The ultrastructural study further found that manykinds of organelles in renal tubular cells were damaged and that main changeswere swelling,degeneration of mitochondria,extensive expansion of endoplasmicreticulum,light loss of microvillus,disappearance of basal folds,dropping ofbound ribosomes from the face of rough endoplasmic reticulum,depolymerizationof polyribosomes,appearance of a great number of autophagic lysosomes andproliferation of renal interstitial tissues.When rabbits accepted daily 120 mg/kg or 30 mg/kg borax during subacuteor chronic exposure to fluoride,boron reduced the adverse effects of fluoride onthe structure of renal tubular cells and their organelles.
出处 《中国地方病学杂志》 CAS CSCD 1992年第3期129-131,共3页 Chinese Jouranl of Endemiology
关键词 氟化钠 硼砂 拮抗作用 肾超微结构 sodium fluoride borax antagonism renal ultrastructure
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