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作 者:张文岚[1] 孙玲[1] 薛立娟[1] 吴岩[2] 李广生[3]
机构地区:[1]吉林大学第一医院器官移植中心,长春130021 [2]吉林大学第一医院干部病房,长春130021 [3]吉林大学地方病研究所
出 处:《中国地方病学杂志》2006年第6期622-624,共3页Chinese Jouranl of Endemiology
基 金:国家自然科学基金重点课题资助项目(39730390)
摘 要:目的探讨营养性低钙与慢性氟中毒细胞内钙超载的相关性。方法采用饮水加入氟化钠进行大鼠染毒实验,配以低钙饮食,应用Fura-2/AM荧光指示剂标记单细胞,显微荧光标记测定慢性氟中毒大鼠肝、肾、脑细胞内游离钙([Ca2+]i)的变化。结果氟可刺激细胞内[Ca2+]i水平增高,正常饮食投氟组肝、肾、脑细胞内[Ca2+]i水平分别为(124.11±11.35)、(127.20±14.40)、(136.75±15.91)nmol/L,与正常饮食对照组(86.37±27.55)、(95.65±8.75)、(99.20±12.89)nmol/L比较,差异有统计学意义(t=4.001、4.706、4.953,P< 0.05);低钙饮食+氟组肝、肾、脑细胞内[Ca2+]i水平[(151.57±19.61)、(162.62±31.41)、(158.79±27.65) nmol/L]与低钙饮食对照组[(103.17±14.29)、(103.59±11.40)、(115.26±30.91)nmol/L]比较,差异有统计学意义(t=4.789,P<0.05;t=8.581、6.003,P<0.01);低钙饮食+氟组骨病变明显:细胞内[Ca2+]i水平与血清离子钙(i[Ca])、总钙(t[Ca])呈负相关(r=-0.59)。结论慢性氟中毒可致机体组织细胞钙超载,低钙可加重氟中毒时的细胞内钙超载,提示细胞内钙超载可能参与氟骨症发病机制并起着重要作用。Objective To explore the relationshipo of low nutritional calcium with over-load of intracellular ionized calcium ([Ca^2+]i) of fluorosis. Methods Wistar rat model was made by feeding sodium fluoride added into drinking water. The Fura-2/AM was employed to measure [Ca^2+]i level in liver, renal and brain tissues of Wistar rats. Results [Ca^2+]i level was obviously increased in the group of high-calcium diet with fluoride than that in the control group of high calcium diet[ (86.37± 27.55), (95.65 ±8.75), (99.20 ±12.89)nmol/L] ; The same changes was observed in the group of low calcium + fluoride and the low calcium group [(124.11± 11.35), (127.20±14.40), (136.75 ± 15.91)nmol/L] (P 〈 0.01 or P 〈 0.05). There was a significant bone damage in the group of low calcium + fluoride. [Ca^2+]i level was negatively correlated with the serum calcium and total calcium concentration (r = - 0.59). Conclusions Fluorosis may result in over-load of intracellular ionized calcium, which could be aggregated by low nutritional calcium. The finding suggested that over-load of intracellular ionized calcium played an important role in the pathogenesis of skeletal fluorosis.
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