Gonadal dysgenesis induced by prenatal exposure to ethinyl estradiol in mice

Yasuda, Yoshiko; Kihara, Takahide; Tanimura, Takashi; Nishimura, Hideo

doi:10.1002/tera.1420320210

Cited by 45 publications

(18 citation statements)

References 17 publications

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“…A mechanism for how oestrogen exposure may affect the meiotic process in female germ cells is indicated in studies of mice which were exposed prenatally to ethinyl oestradiol ovarian germ cell (Yasuda et al, 1977;Yasuda et al, 1985). A reduced number of follicular cells and normal primordial follicles as well as an increased number of degenerating follicles were found in Matched the ovaries of mice whose mothers were treated on days 1 1-OR 95% CL 17 of gestation.…”

Section: Matchedmentioning

confidence: 99%

Hormonal factors and risk of ovarian germ cell cancer in young women

Walker

Ross²,

Haile³

et al. 1988

Br J Cancer

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Summary No previous controlled studies of ovarian germ cell tumours have been reported; however the tumour is similar to germ cell testicular cancer in terms of histology, age-specific incidence rates (i.e. highest rates in young adulthood), and secular trends of increasing incidence. The investigation was designed to determine if maternal hormonal factors which have been found to increase the risk of testis cancer in male offspring are also risk factors for the ovarian tumour. The analysis is based on 73 cases diagnosed before age 35 and 138 age-race matched controls. The cases were identified by tumour registries in Los Angeles and Seattle Ovarian germ cell cancer is quite rare and no previous controlled epidemiologic studies have been reported. The similarity of these tumours to germ cell testicular cancer in terms of histology (Teilum, 1976), age-specific incidence rates highest in the young adult age range (Walker et al., 1984; Weiss, 1982), and secular trends of increasing incidence (Walker et al., 1984) Angeles case series and 15 were from Seattle.For each case an attempt was made to identify two ageand race-matched controls using friends or neighbours so as to approximate a socioeconomic match. For cases under age 18 at diagnosis, the controls were selected from friends or neighbours of the case in the year prior to diagnosis. For cases over age 18 at diagnosis, controls were selected from among the case's friends or neighbours at the time of graduation from high school, in order to approximate the social class of the case's mother rather than of the case herself.The procedure for obtaining the potential friend control names was to ask the case mother for a list of first names of friends of the case from the appropriate time period at the beginning of the interview and to have her rank them according to closeness in friendship and age to the case. Then at the end of the interview, permission was requested to contact these friends, beginning with the first two ranked friends who were within two years of the case's age and of the same race.Neighbourhood controls were sought when two friend controls could not be identified. The neighbourhood controls were selected by following a specified walking pattern in the blocks around the case's residence. Residents of each unit were surveyed until a race and age (±5 years) match was located.Once the control was selected, permission was sought to interview her mother. At least one control mother interview was completed for 73 of the 74 cases whose mothers were interviewed, and two or more were obtained for 54 cases. For 20 cases, only neighbourhood control mothers were used, and in 8 cases both friend and neighbourhood control mothers were used. In total, 138 control mothers were interviewed, 93 from friends and 45 from neighbourhood residents. Three potential friend controls and 10 qualifying neighbourhood controls refused to participate.

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Section: Matchedmentioning

confidence: 99%

Hormonal factors and risk of ovarian germ cell cancer in young women

Walker

Ross²,

Haile³

et al. 1988

Br J Cancer

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“…Testicular maldescent can be produced experimentally in animals by administering diethylstilbestrol (DES) or other forms of oestrogen during gestation (Jean, 1973;McLachlin et al, 1975;Nomura & Kanzaki, 1977;Yasuda et al, 1985). A number of clinical studies have found an increased frequency of cryptorchidism in males with a history of DES exposure in utero (Cosgrove et al, 1977;Whitehead & Leiter, 1981).…”

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confidence: 99%

Maternal hormone levels in early gestation of cryptorchid males: a case-control study

Bernstein

Pike²,

Depue³

et al. 1988

Br J Cancer

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Summary A case-control study was conducted to assess maternal hormonal factors associated with increased risk of bearing a cryptorchid son. Serum samples were collected during the first trimester of pregnancy from participants in the US Collaborative Perinatal Study. Twenty-five mothers of normal offspring (controls) were individually matched on medical center, age, parity, weight and length of gestation at the time of sampling to women bearing sons who had a diagnosis of cryptorchidism at one year of age or older. Compared with controls, mothers of cryptorchid sons (cases) had significantly greater percentages of non-protein bound (P=0.010) and albumin-bound (P=0.014) estradiol during the first trimester of the index pregnancy. On average, cases had 16% more bioavailable oestradiol than controls. Levels of human chorionic gonadotropin, testosterone, non-protein bound testosterone and sex-hormone binding globulin did not differ between the two groups. The data presented support the hypothesis that cryptorchidism results from elevated maternal oestrogen levels early in pregnancy.

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“…34 The same associations have been suggested in humans, 38 although they are still under debate. 39 Sons of women who themselves were exposed in utero to diethylstilbestrol (DES), may have an elevated risk of TC although the data are not unequivocal.…”

Section: The Oestrogen Hypothesismentioning

confidence: 54%

“…Exposure of pregnant mice to oestrogens has been found to increase the frequency of testicular dysgenesis 34 , cryptorchidism 35 , hypospadias 36 and TC 37 in male offspring; and there is also evidence of impaired Leydig cell development and reduced Sertoli cell numbers, resulting in impaired spermatogenesis. 34 The same associations have been suggested in humans, 38 although they are still under debate.…”

Section: The Oestrogen Hypothesismentioning

confidence: 99%