| Objective By studying thyroid function and morphology,bone mass,bone remodeling,bone histomophormetry and transcriptional level of specific gene of osteoblast and osteoclast in long-term high iodine intake Wistar rats,mechanism of excessive iodine-thyroid hormone-bone metabolism will be preliminarily discussed.With definition of hazards on bone metabolism caused by excessive iodine,this experiment provides reference data for scientific and permanent implementation of Universal Salt Iodization(USI)in China.Methods Wistar rats(1 month after weaning),half male and half female,were random divided into five groups by body weight:nomal iodine(NI),five-fold high iodine(5HI),ten-fold high iodine(10HI),fifty-fold high iodine(50HI)and one hundred-fold high iodine(100HI).Each group were feed with normal iodine feeds(iodine content:296.1×7.9?g/kg).Rats of NI group drank tap water(iodine content:7.6?g/L)and those of high iodine groups drank water containing different content of potassium iodate,which was 820?1845?10045?20295?g/L respectively.Body weight of all rats were weighed each week.24h urinary iodine were determined with rsenic-cerium catalytic spectrophotometry in the 1st,5th and 9th month.Rats were sacrificed in the 6th and 12th month,level of serum free triiodothyronine(FT3),free thyroxine(FT4)and sensitive thyroid stimulating hormone(sTSH)of all rats were measured with chemiluminescence immunoassay,while serum triiodothyronine(T3)and thyroxine(T4)were measured with radioimmunoassay;bone mineral density(BMD)were measured by dual energy X ray absorptiometry,while pathological changes of thyroid and trabecular were observed with HE staining at the same time.In the 12th month,bone mineralization apposition rate of each group were measured with tetracycline hydrochloride-calcein double labeling method,transcription level of RUNX2,OCN in osteoblast and MMP-9,CtsK in osteoclast were determined with real-time PCR(RT-PCR).Results 1.Body weight of each group maintained increasing.Urinary iodine levels increased with increasing iodine intakes(P<0.01).2.Differences of T3,T4,T3/T4,FT3,FT4 and sTSH between 6th and 12th month was not significant,while T3,T4,T3/T4,FT3 and FT4 increased gradually.In the 12th month,sTSH of male rats in high iodine groups was significantly higher than NI(P<0.01).3.Thyroid gland cells of high iodine rats showed follicular hyperplasia,while fused follicles and colloid retention appeared in parts of individuals;As intervention dose and time increased,follicular hyperplasia and vacuoles in epithelial cells appeared more obvious,which suggested existence of TSH stimulation in thyroid gland.4.BMD of each group tended to decrease with iodine intake increasing at 6th month,while BMD of male rats in 5HI and 10HI was significantly lower than NI rats(P<0.01).5.In the 6th month,bone trabecular in high iodine groups were rare and thinned,hematopoietic cells were reduced while fat vacuole increased in bone marrow.In the 12th month,trabecular structure lesions progressed,a large number of fat vacuole filled bone marrow,especially in 50HI and 100HI.6.Distance between double lebeling lines and MAR in high iodine groups decreased significantly(P<0.01)with increasing iodine intakes.Double labeling lines were dispersed with apparent dislocation.7.Transcription levels of RUNX2,OCN,MMP-9 and CtsK in high iodine groups increased significantly(P<0.01)compared with NI rats.Conclusion 1.Long-term excessive iodine intake may result in hyperthyroidism and polymorphous histological changes in Wistar rats' thyroid gland tissue;2.long-term excessive iodine intake leads to defects in mineralization,which would suppress normal bone remodeling of adult rats;besides,changes of bone mass and bone microarchitetructure also suggested long-term excessive iodine may lead to severe endocrinal osteoporosis.Therefore,bone metabolism disturbance caused by excessive iodine should be highly emphasized. |
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