Impact of congenital or experimental hypogonadotrophism on the radiation sensitivity of the mouse ovary

被引:70
作者
Gosden, RG
Wade, JC
Fraser, HM
Sandow, J
Faddy, MJ
机构
[1] Univ Leeds, Ctr Reprod Growth & Dev, Leeds, W Yorkshire, England
[2] Univ Edinburgh, Sch Med, Dept Physiol, Edinburgh EH8 9AG, Midlothian, Scotland
[3] MRC, Reprod Biol Unit, Edinburgh EH3 9EW, Midlothian, Scotland
[4] Hoechst AG, D-6230 Frankfurt, Germany
[5] Univ Queensland, Dept Math, Brisbane, Qld 4072, Australia
关键词
follicle; gonadotrophin-releasing hormone; mouse; ovary; radiation;
D O I
10.1093/humrep/12.11.2483
中图分类号
R71 [妇产科学];
学科分类号
100211 ;
摘要
As the numbers of young people making a full recovery from haematological malignancy continue to rise, reproductive science must investigate ways of ameliorating the sterilizing effects of high-dose chemotherapy and total body irradiation. Because there is conflicting evidence as to whether lower serum gonadotrophin concentrations have any protective effect on the gonads, a study was designed to test whether either congenital or experimentally induced hypogonadism reduces the radiosensitivity of the mouse ovary. Test subjects were either homozygous for the hpg locus or animals of normal phenotype treated with a gonadotrophin-releasing hormone antagonist. At 14 days after receiving a single dose of 0.1, 0.2 or 0.3 Gy X-rays or a sham procedure, primordial follicles in the ovaries of the two experimental groups and controls were counted in serial histological sections. The doses at which half of the follicles were lost (LD50) were estimated as 0.11 +/- 0.02, 0.19 +/- 0.02 and 0.17 +/- 0.02 Gy respectively. There was no significant difference between the controls and the antagonist-treated animals, but the congenitally hypogonadal group was unexpectedly more sensitive to radiation. Either way, these results do not support the hypothesis that the ovary is protected from radiation injury by lower gonadotrophin concentrations.
引用
收藏
页码:2483 / 2488
页数:6
相关论文
共 38 条
[1]   MECHANISM AND MANAGEMENT OF TREATMENT-RELATED GONADAL FAILURE IN RECIPIENTS OF HIGH-DOSE CHEMORADIOTHERAPY [J].
APPERLEY, JF ;
REDDY, N .
BLOOD REVIEWS, 1995, 9 (02) :93-116
[2]   LUTEINIZING-HORMONE-RELEASING HORMONE AGONIST INHIBITS CYCLOPHOSPHAMIDE-INDUCED OVARIAN FOLLICULAR DEPLETION IN RHESUS-MONKEYS [J].
ATAYA, K ;
RAO, LV ;
LAWRENCE, E ;
KIMMEL, R .
BIOLOGY OF REPRODUCTION, 1995, 52 (02) :365-372
[3]   IS RADIATION-INDUCED OVARIAN FAILURE IN RHESUS-MONKEYS PREVENTABLE BY LUTEINIZING-HORMONE-RELEASING HORMONE AGONISTS - PRELIMINARY-OBSERVATIONS [J].
ATAYA, K ;
PYDYN, E ;
RAMAHIATAYA, A ;
ORTON, CG .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 1995, 80 (03) :790-795
[4]  
ATAYA KM, 1985, CANCER RES, V45, P3651
[5]  
ATAYA KM, 1988, CANCER RES, V48, P7252
[6]   SUCCESSFUL PREGNANCY AFTER ALLOGENEIC BONE-MARROW TRANSPLANTATION FOR CHRONIC MYELOID-LEUKEMIA [J].
ATKINSON, HG ;
APPERLEY, JF ;
DAWSON, K ;
GOLDMAN, JM ;
WINSTON, RML .
LANCET, 1994, 344 (8916) :199-199
[8]  
BEAUMONT HM, 1969, RADIATION BIOLOGY FE, P943
[9]  
Blumenfeld Z, 1996, HUM REPROD, V11, P1620
[10]   PROTECTIVE EFFECTS OF D-TRP6-LUTEINIZING HORMONE-RELEASING HORMONE MICROCAPSULES AGAINST CYCLOPHOSPHAMIDE-INDUCED GONADOTOXICITY IN FEMALE RATS [J].
BOKSER, L ;
SZENDE, B ;
SCHALLY, AV .
BRITISH JOURNAL OF CANCER, 1990, 61 (06) :861-865