Attempted Protection of Spermatogenesis From Single Doses of Gamma-Irradiation in the Androgen Pretreated Rat

Schlappack, O; Delic, Julian I.; Harwood, Janet R.; Stanley, Judith A.

doi:10.3109/01485018708986827

Cited by 9 publications

(2 citation statements)

References 15 publications

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“…within 10 days and sperm are produced within 6-8 weeks after irradiation or chemotherapy ( L u et al 1980;Meistrich et al 1982;van der Meer et al 1992;Meistrich 1993). The rat appeared more sensitive than the mouse to damage produced by irradiation, and certain rat strains are more sensitive than others (Delic et al 1987). For example, LBNF, rats show a complete failure of spermatogenic cell differentiation for one year after only 3.5 Gy of irradiation (Kangasniemi et al 1996b).…”

Section: Failure Of Recovery Of Spermatogenesis From Surviving Stem Cmentioning

confidence: 99%

Hormonal stimulation of the recovery of spermatogenesis following chemo‐ or radiotherapy

Meistrich

1998

APMIS

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Meistrich, M. L. Hormonal stimulation of the recovery of spermatogenesis following chemo-or radiotherapy. APMIS 106: 3 7 4 6 , 1998.Radiation and chemotherapeutic drugs produce prolonged depression of sperm counts in rodents and humans. Previously, three approaches have been developed in experimental animals that have had some success in preventing or reversing this toxicity. These approaches included pretreatment with hormones that suppress spermatogenesis, stimulation of stem cell number, and supplementation with testosterone. A different rationale for the ability of particular hormonal treatments to reverse prolonged azoospermia is presented in this review. In many cases prolonged azoospermia occurs even though the stem spermatogonia survive the toxic insult, but the differentiation of these spermatogonia to produce sperm fails. In the rat, the block appears to be at the differentiation of the A spermatogonia. Hormone treatments with testosterone or with GnRH agonists, which suppress intratesticular testosterone levels, relieve this block and result in the production of differentiating cells. When the hormone treatment is stopped the production of differentiating cells continues, mature sperm are produced, and fertility is restored. If a similar mechanism can be demonstrated to hold in humans, the fertility of men who have been rendered infertile by treatments for testicular and other cancers could be improved.

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Section: Failure Of Recovery Of Spermatogenesis From Surviving Stem Cmentioning

confidence: 99%

Hormonal stimulation of the recovery of spermatogenesis following chemo‐ or radiotherapy

Meistrich

1998

APMIS

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“…The prevention of gonadal damage during radiotherapy is therefore a major concern. Since shielding the testes offers only poor protection to spermatogenesis, various other experimental approaches, aimed at preventing radiation-induced quantitative damage to the gonads, have been explored (2)(3)(4)(5)(6)(7)(8). Some of these have achieved protection of testicular function to various degrees (2)(3)(4)(5)8).…”

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Protective effect of medroxyprogesterone acetate plus testosterone against radiation-induced damage to the reproductive function of male rats and their offspring.

Jégou

Calle

Bauché

1991

Proc. Natl. Acad. Sci. U.S.A.

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This study attempted to protect spermatogenesis and the reproductive performance of rats against the effects of acute scrotal exposure to x-rays. Daily subcutaneous hnjections of medroxyprogesterone acetate (8 mg/kg) plus testosterone (1 mg/kg) (MT group) were administered for 55 days (experiment A) or 15 days (experiment B). The rats were irradiated (3 grays) on the last day of MT pretreatment (MTX group). In both experiments, on days 1 and 130 posttreatment, rats from each of the four groups (control, x-irradiated, MT, and MTX groups) were killed to measure the weight of the reproductive organs and the number of epididymal spermatozoa. Breeding was started 3 days posttreatment by housing all males from the four groups each with two irgin females for six successive periods of 19 days, separated by a period of 2 days.The percentage offertile males, the litter size, postimplantation losses, and dominant lethal mutations were calculated. In experiment A, in the last fertility trial, animals of both sexes were selected at random from the progeny of each group (FI).When they were adults, their fertility was tested in a mating trial. A fertility trial was also performed with the F2 males. Our data essentially reveal that (i) in addition to their adverse quantitative effects on spermatogenesis, x-rays also produce a significant increase in dominant lethal mutations in all germ cell classes, including stem spermatogonia; (ii) the F1 and F2 male descendants of irradiated male rats provoked abnormal rates of postimplantation losses in their female mates; (iii) the short as well as the long MT pretreatment protects testicular function of irradiated rats; and (iv) in experiment A, MT pretreatment totally prevented qualitative damage to spermatozoa and protected the descendants of the irradiated animals against altered spermatogenesis as well as against genetic damage in germ cells. In conclusion, pretreatment with MT, even for a short period of time, offers a method for potentially reducing the toxic and genotoxic effects of irradiation on the male reproductive system. Radiation has particularly severe adverse effects on spermatogenesis and therefore on fertility in both animals and man (1). Radiation therapy is nevertheless widely used because there is often no other choice for the treatment of a number of cancers in children and adults. The prevention of gonadal damage during radiotherapy is therefore a major concern. Since shielding the testes offers only poor protection to spermatogenesis, various other experimental approaches, aimed at preventing radiation-induced quantitative damage to the gonads, have been explored (2-8). Some of these have achieved protection of testicular function to various degrees (2-5, 8). However, a major limitation of these studies is that the reproductive performances of the experimental animals and of their progeny was not assessed. It is known that in addition to azoo-or oligozoospermia, radiation also produces germ-line mutations leading to inherited anomalies in rodents (9-13) an...

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Response of the seminiferous epithelium to scattered radiation in seminoma patients

Schlappack

Kratzik

Schmidt

et al. 1988

Cancer

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Semen and blood samples were obtained, at 3-month intervals over 12 to 28 months, from patients who underwent subdiaphragmal radiation after orchidectomy for seminoma testis. Before radiotherapy a mean (+/- SE) semen volume of 4.7 +/- 0.5 ml, a mean sperm count of 44.4 +/- 13.5 x 10(6)/ml, a mean percentage of motile cells of 20.3 +/- 5.2, a mean percentage of morphologically normal spermatozoa of 13.4 +/- 5.4, a mean percentage of swollen sperm of 39.6 +/- 7.4, and a mean serum follicle-stimulating hormone (FSH) value of 8.3 +/- 1.2 mIU/ml was found. The mean testicular dose from scatter was 62 +/- 5 cGy (range, 34 to 95 cGy). Sperm counts between 0 and 2.75 x 10(6)/ml were seen at 6.8 +/- 0.6 months and recovery to values greater than 2.25 x 10(6)/ml at 11.8 +/- 0.8 months after the start of radiation. Peak FSH values of 19.2 +/- 1.6 mIU/ml were obtained at 6.7 +/- 0.9 months after the start of irradiation. After recovery mean semen volume was 3.9 +/- 0.4 ml, mean sperm count 34.6 +/- 5.6 x 10(6)/ml, the mean percentage of motile cells 42.5 +/- 6.0, the mean percentage of swollen sperm 58.7 +/- 6.8, and the mean percentage of spermatozoa with normal morphology 23.4 +/- 5.1. Only motility was significantly different (P less than 0.01) from pretreatment values. The elevation of FSH values with time after start of radiotherapy reflected the toxicity to spermatogenesis but no correlation was found between peak FSH levels and scattered radiation dose. Also, neither the time from start of radiotherapy to sperm count nadir or recovery nor the time to peak FSH levels was significantly correlated with radiation dose.

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Attempted Protection of Spermatogenesis From Single Doses of Gamma-Irradiation in the Androgen Pretreated Rat

Cited by 9 publications

References 15 publications

Hormonal stimulation of the recovery of spermatogenesis following chemo‐ or radiotherapy

Hormonal stimulation of the recovery of spermatogenesis following chemo‐ or radiotherapy

Protective effect of medroxyprogesterone acetate plus testosterone against radiation-induced damage to the reproductive function of male rats and their offspring.

Response of the seminiferous epithelium to scattered radiation in seminoma patients

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