Protection from Radiation-Induced Damage to Spermatogenesis by Hormone Treatment

Kurdoglu, Belma; Wilson, Gene; Parchuri, Nandakishore; Ye, Wei-San; Meistrich, Marvin L.

doi:10.2307/3578738

Cited by 56 publications

(20 citation statements)

References 22 publications

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“…The mechanism behind the secondary decline is not known, but our recent results suggest that the mechanism may be under endocrine regulation and can be manipulated by hormone treatment. In LBNF 1 rats, suppression of LH and intratesticular testosterone levels by testosterone plus estradiol treatment prior to irradiation markedly improved recovery of spermatogenesis at 10 wk following a single 3.5-Gy dose of irradiation [13]. We propose that hormone treatment affected the recovery from stem cells after irradiation.…”

Section: Recovery Of Spermatogenesismentioning

confidence: 82%

“…In contrast to Sprague-Dawley rats, in which more than 95% of tubules show repopulation after doses of [3][4] in LBNF, rats only 12% of tubules recover after 3 Gy [13]. Similarly, after treatment with procarbazine, another agent known to kill stem spermatogonia, LBNF, rats show poorer recovery of spermatogenesis than do Sprague-Dawley rats [14].…”

Section: Introductionmentioning

confidence: 95%

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Failure of Spermatogenesis to Recover Despite the Presence of A Spermatogonia in the Irradiated LBNF1 Rat1

Kangasniemi

Huhtaniemi

Meistrich

1996

Biology of Reproduction

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112

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The dose and time response of LBNF1, rat testis to gamma irradiation was studied with use of single doses from 2.5 Gy to 6.0 Gy. Germ cells were initially depleted as a result of killing the radiosensitive differentiating spermatogonia. Some recovery of spermatogenesis was observed at 4 and 6 wk after irradiation as indicated by the repopulation of tubules with germ cells derived from surviving stem spermatogonia. Although spermatogenesis showed additional recovery and was maintained throughout the 60-wk follow-up period after 2.5 Gy, at doses from 3.5 Gy to 6.0 Gy, repopulation indices declined after 6 wk to less than 2%. The numbers of Sertoli cells per nonrepopulating tubule were constant, independent of radiation dose or time. In addition, the nonrepopulating tubules contained an average of one A spermatogonium per 100 Sertoli cells. The size and shape of these cells corresponded to undifferentiated A spermatogonia in nonirradiated control tests. Despite high labeling (40%) and mitotic (20%) indices, the numbers of A spermatogonia changed very little with time, and no differentiated cells were produced in these tubules. The failure of spermatogenesis to recover was not due to hormone deficiency: serum gonadotropin levels increased after irradiation, and serum testosterone remained at control levels. The irradiated LBNF1 rat model may be useful for studying the regulation of differentiation of A spermatogonia.

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Section: Recovery Of Spermatogenesismentioning

confidence: 82%

Section: Introductionmentioning

confidence: 95%

Failure of Spermatogenesis to Recover Despite the Presence of A Spermatogonia in the Irradiated LBNF1 Rat1

Kangasniemi

Huhtaniemi

Meistrich

1996

Biology of Reproduction

Self Cite

112

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“…In each preparation, at least 200 sperm was counted. This motility assessment was repeated in a new preparation from the same semen sample (Kurdoglu et al, 1994).…”

Section: Sperm Parameters Assessmentmentioning

confidence: 99%

Maternal Water Deprivation Affects the Spermatogenesis of the Offspring Rats

2013

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SUMMARY:Prenatal stresses such as water deprivation affect developmental process of embryo. This study evaluated the effects of water deprivation in pregnant mother on histological parameters of testis of offspring. Pregnant rats were divided into two groups (control and experimental). In experimental animals, water was removed from the ewes for 48h at the end of third trimester of gestation (19-21th days). Histopathology and histomorphic analysis and also TUNEL assay on offspring's testes were performed at pubertal age (60 days). The sperm motility either compared between two groups. The results showed that prenatal water deprivation induced histopathological alteration such as epithelium vacuolization, sloughing and detachments (P<0.01). Morphometrical data showed that prenatal water deprivation decreased tubular diameter and reduce epithelium height (P<0.01). Johnsen's score showed poor spermatogenesis in experimental group (P=0.001). The percent of germ cell apoptosis was increased in offspring's testes of rats born to mothers exposed to stress during pregnancy (P=0.000). The increased number of Multinucleated cells in the seminiferous lumen (P=0.000) in parallel with decreased number of sertoli cells (P=0.03) showed adverse effect of prenatal water deprivation on blood testis barrier. Present study revealed that prenatal water deprivation had injurious effect on developmental process of testes that affects on both germ cells and sertoli cells and had noxious effect on sperm parameters. These data confirm that prenatal stress disrupts normal spermatogenesis of offspring.

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“…Increased stem cell survival was evident by 50 days, and at 90 days sperm count was close to normal and significantly higher than it was in rats treated with procarbazine alone. Similar protective effects of hormonal treatment have been described following the use of testosterone [37], testosterone and estradiol [38], GnRH and testosterone [39], and GnRH and the antiandrogen flutamide [40,41], following gonadal insult with procarbazine, cyclophosphamide, or radiotherapy. Pogach et al [39] suggested that testosterone administered after treatment with procarbazine enhanced the recovery of spermatogenesis.…”

Section: Hormonal Manipulationmentioning

confidence: 63%

Fertility preservation and management of gonadal failure associated with lymphoma therapy

Howell¹,

Shalet

2002

Curr Oncol Rep

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Treatment with cytotoxic chemotherapy and radiotherapy is associated with significant gonadal damage in men and women. The likelihood of gonadal failure following cytotoxic chemotherapy is dependent on the drug and dose, and in women there is also an effect of age at treatment. Irradiation of the testes or ovaries, either directly or indirectly, is also a significant cause of gonadal dysfunction, and the potential to recover from damage is clearly related to the radiation dose received. Several methods of preserving gonadal function during potentially sterilizing treatment have been considered. At present, sperm banking remains the only proven method in men, although hormonal manipulation to enhance recovery of spermatogenesis and cryopreservation of testicular germ cells are possibilities for the future. Transposition of the ovaries to allow better shielding during radiotherapy is of use in some women, and the prospect of cryopreservation and reimplanation of ovarian tissue appears to be promising.

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Protection from Radiation-Induced Damage to Spermatogenesis by Hormone Treatment

Cited by 56 publications

References 22 publications

Failure of Spermatogenesis to Recover Despite the Presence of A Spermatogonia in the Irradiated LBNF1 Rat1

Failure of Spermatogenesis to Recover Despite the Presence of A Spermatogonia in the Irradiated LBNF1 Rat1

Maternal Water Deprivation Affects the Spermatogenesis of the Offspring Rats

Fertility preservation and management of gonadal failure associated with lymphoma therapy

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