Abstract: Objective To observe influences of fluorosis caused by coal burning on ovarian reproductive function in female rats.Methods Female Sprague-Dawley rats in experiment group were fed with corn roasted with raw coal from Zhijin area,an endemic fluorosis area,to establish an animal model of coal-burning fluorosis.The changes of the teeth of the female rats during fluorine exposure was observed.Fluorine contents of urine and bone were detected.The ovaries of the rats were collected and ovary coefficient was calculated;the pathological morphology of ovary,the changes of ovarian follicles at different development stage,and the number of corpus luteum were observed with light microscope.Estrus female rats were sacrificed at different time(60,120,180 days)of the fluoride exposure to collect serum samples for the determination of estradiol(E₂)with radioimmunoassay.Results Compared with the control group,the fluorine contents of urine and bone increased significantly with the increment of fluoride exposure time in the experiment group.In the fluoride exposure group,all follicular granulosa cells showed progressive edema;atresia of the follicle and degradation of corpus luteum increased gradually and mature follicle were observed occasionally.Compared with the control group,the number of atresia follicles significantly increased in moderate fluoride exposure group(24.000±4.138 at 180 day)and in high fluride exposure group(24.200±3.705 at 120 day and 25.000±4.714 at 180 day)(P<0.05 for all).Compared with the control group,serum estradiol levels in the rats in moderate fluoride exposure group(43.875±7.180 pmol/L)and high fluoride exposure group(45.625±5.780 pmol/L) increased at 60 day of the experiment(P<0.05 for all).Conclusion There are toxic effects of coal-burning fluorosis on the ovary of female rasts and the mechanism of the effects is related to the increases of follicle degeneration and atresia of follicles at different stages,follicular granulosa cell edema,damage of follicular cells,and the impaired synthesis and secretion of E₂.