大鼠实验性氟肝病

Experimental Fluorohepatopathy of Rats

本文以光镜、电镜和酶组织化学方法观察了大鼠低超常量(5ppm F^-)慢性氟中毒时的肝脏病变及其早期动态变化。1.8只非纯系雌性幼龄大鼠自由饮用含氟量为5ppm 的脱离子水13个月后,发现①肝细胞胞浆呈缺氧性超微变化。②肝细胞脂肪变和点灶性坏死。③肝细胞再生活跃。④肝贮脂肪细胞增生。⑤肝间质细胞增生、胶原纤维增生并呈早期肝纤维化趋势;2.30只 SD 雌性幼龄大鼠自由饮用含氟量为5ppm 的脱离子水2、4和6个月后各处死10只,发现了与上述慢性氟中毒大鼠相似的肝脏病变;酶组织化学观察表明,4和6月氟中毒大鼠肝细胞的 Mg^(++)-ATPase、SDH、G-6-P 和 G-6-PDH 的活性都低于对照组。本文的大鼠实验性氟肝病是以近乎国内高氟区人群饮水氟含量的条件诱发的,故应对高氟区人群的肝脏情况予以关注。

Eight young female rats freely drank fluoridized water containing 5ppm F^- for 13months,so animal model of chronic fluorosis was established.As a control,anotherfour rats freely drinking running water were used.Light and electron microscopicobservations showed the following lesions in the livers:(1) fatty change,focal nerco-sis,and cholestasis of the hepatocytes;(2)active hepatocyte proliferation;and (3)prominent cell proliferation,and a tendency towards early hepatic fibrosis.Other 30young female rats drinking the same fluoridized water were killed at the end of 2nd,4th,and 6th months of the experiment respectively (10 in each group);as comparedwith the corresponding control rats (10 in each group) drinking running water,theexperimental animals showed similar morphologic changes as described above.In theearly dynamic cytochemical studies on injuried hepatocytes,decreased activity ofSDH,G6Pase,G6PDH,Mg^(2+)-ATPase were noticed.The results indicate NaF is a li-mitative hepatotoxicant.Because the induced concentration of F^- is similar to thatin some areas of endemic fluorosis,it must be emphasized the problem of the liverof the population in the endemic areas.