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.
出处
《中国地方病学杂志》
CAS
CSCD
北大核心
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)
关键词
钙
氟
中毒
细胞内钙超载
Calcium
Fluorine
Poisoning
Over-load of intracellular ionized calcium
