| There were two experiments in the present study. In experiment I , 250 one-day chicken were randomly divided into 5 groups,50 for each group. Group I was the control, groupll,III,IV,V were fed the diets containing 500,1000,1500,2000 mg/kg of fluorine as sodium fluoride, respectively, for 150 days; The models of fluorostic chicken were established and a series of indexes reflecting free radical changes , antioxidations ,the structure and function of erythroeytic membrane ,thyroid and liver was determined ,one hand ,to clarify the mechanism of fluoride-induced damages to the whole organism, erythrocytic membrane, thyroid and liver at molecular level and from the aspect of fluoride disturbing the metabolism of free radicals and the functions of antioxidant defense system , on the other hand, to sift the specific or reliable indexes of early diagnosing fluorosis and to get the normal value of fluorine in some tissues.In experiment II, the experimental animals and duration were same as the experiment I Group I was the control, group II, III, LV, V were ,respectively ,fed the diets containing excessive fluoride ,deficient selenite, excessive fluoride with deficient selenite, and excessive fluoride with supplemental selenite. The animal models of selenium deficiency , fluorosis together with selenium deficiency , fluorosis with supplementary selenite were established to clarify the biological correlation among fluorine , selenium and iodine.The results indicated as follows:1 .All the experimental animal models were successfully established.2.The molecular mechanism of fluorosis in chicken is that fluorine induces excessive oxygen, nitrogen free radical(NO) and lipid peroxides(LPO),disturbs the free radical metabolism, reduces the function of scavenging free radicals and antioxidant defense system in organism, which results in strongly oxidant stress, furthermore, injures the structure and function of all tissues and organs , damages to the metabolism process and causes a series of pathological changes, which contributes to the pathogenesis of fluoride-induced injury in organism.3.Excessive fluorine affects the metabolism of ATPase and SA in erychrocytic membrane , and decreases the activity of ATPase and the contents of sialic acid (SA) ,which can partially explain the mechanism of anemia due to fluorosis.4.The structure and function of liver were hurted due to the excessive fluoride ingestion.5 .Excessive fluorine induces thyroid atrophia in short time, however, prolonged excessive fluoride ingestion causes thyroid enlargement which is nodular and colloid goiter. Fluoride injures the structure and function of thyroid and liver, and the ultralstructure of thyroid,disturbs the synthesis and secretion of thyroid hormone, interferes with the regulatory system of thyroid. The mechanism of fluoride-induced injury in erythrocyte, thyroid and liver is that fluoride results in disorder of free radial metabolism, excessive free radicals and LPO in organism damages to tissue and cell biological membrane structure and the metabolism of biological molecular,therefore, the structure and function of erythrocyte, thyroid follicular cell and hepatocyte were abnormal.6.The normal reference value of fluorine contents in some tissues were established.7.The ratio of SA and glycosaminoglyean (SA/GAG) reducing by 30% or more in sera can be employed as a more sensitive , more reliable, and earlier index for diagnosing fluorosis , which can provide scientific basis for rightly diagnosing and treating fluorosis.8.In some degree, Selenium deficiency and fluorosis both can decrease the activity of thyroid ingesting iodine. Selenium deficiency slightly injures the ultrastructure of thyroid and dose not cause goiter. Compared with selenium deficiency, fluorosis is more essential factor causing goiter and ultralstructure damage to thyroid. Selenium can accelerate the excretion of fluorine from tissues, antagonize fluoride-induced damage to thyroid and antioxidant defense system, therefore, being kept prope...
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