Duration of spermatogenesis in the mouse and timing of stages of the cycle of the seminiferous epithelium

Oakberg, E.F.

doi:10.1002/aja.1000990307

Cited by 892 publications

(447 citation statements)

References 8 publications

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“…The time (day) between defined spermatogenic stages was adopted from the literature [34,37] and was used to estimate the irradiated precursors of collected cell types. All cell types collected from mice treated at 6-d/o were from irradiated primitive type A spermatogonia.…”

Section: Sensitivity Of Spermatogenic Cells To Mutagenesis By Irmentioning

confidence: 99%

Recovery of a low mutant frequency after ionizing radiation-induced mutagenesis during spermatogenesis

Intano

McCarrey

et al. 2008

Mutation Research/Genetic Toxicology and Environmental Mutagene

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Humans are exposed to ionizing radiation (IR) under various circumstances, e.g. cosmic radiation, diagnostic X-rays and radiotherapy for cancer. It has been shown that IR can impair spermatogenesis and can cause mutations in germ cells. However, the mutagenic responses of germ cells exposed to IR at different stages of testicular maturation have not been examined by directly assessing the mutant frequency in defined spermatogenic cell types. This study was performed to address whether preadult exposure to IR can increase mutations in adult germ cells that could in turn have a major impact on adult reproductive function and the health of ensuing offspring. Male Lac I transgenic mice were irradiated with a single dose of 2.5 Gy of γ-ray at different ages before adulthood, reflecting different stages of testicular maturation, and then mutant frequency (MF) was determined directly in spermatogenic cell types emanating from the irradiated precursor cells. The results showed that (1) preadult exposure to IR did not significantly increase MF in adult epididymal spermatozoa; (2) spermatogenic stages immediately following the irradiated stage(s) displayed an elevated mutant frequency, but (3) the mutant frequency was restored to unirradiated levels in later stages of spermatogenesis. These findings provide evidence that there is a mechanism(s) to prevent spermatogenic cells with elevated mutant frequencies from progressing through spermatogenesis.

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Section: Sensitivity Of Spermatogenic Cells To Mutagenesis By Irmentioning

confidence: 99%

Recovery of a low mutant frequency after ionizing radiation-induced mutagenesis during spermatogenesis

Intano

McCarrey

et al. 2008

Mutation Research/Genetic Toxicology and Environmental Mutagene

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show abstract

“…Testis.-The cell-cycle kinetics of spermatogenesis in the mouse testis have been studied extensively (Oakberg, 1956;Meistrich et al, 1978). While the response of spermatogonial stem cells will determine long-term sterility, this population in the testis of the mouse shows considerable resistance to most chemotherapeutic agents.…”

Section: Tumour Systemsmentioning

confidence: 99%

“…alkylating agents by misonidazole (1-[2-nitromidazole-1 -yl] -3 -methoxypropan -2-ol) (MISO) has been reported for several mouse tumour systems by many authors (Rose et al, 1980;Tannock, 1980;Clement et al, 1980;Martin et al, 1981;Law et al, 1981;Siemann, 1981;Stephens et al, 1981;Twentyman et al, 1981;AMulcahy et al, 1981). Most of these studies have shown that, at least under some circumstances, MISO is more effective in increasing the cytotoxicity of chemotherapeutic agents to tumours than to normal tissues, thereby giving a positive therapeutic gain, though there is no clear consensus as to the mechanisms involved.…”

mentioning

confidence: 99%

Enhancement of CCNU cytotoxicity by misonidazole: possible therapeutic gain

Hirst¹,

Brown²,

Hazlehurst³

1982

Br J Cancer

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Summary.-Enhancement of CCNU cytotoxicity by misonidazole (MISO) was studied in three tumours and two normal tissues in the mouse.The 3 experimental tumours (SCCVII/St, EMT6 and KHT) showed very different sensitivities to CCNU alone, but MISO enhanced the cell killing in ech case. The effect was not always dose-modifying, so that the CCNU dose range for the greatest enhancement was different in each of the tumours. In all 3 tumours, enhancement increased with dose of MISO.The effect on two normal tissues, marrow (CFU-S) and testis (spermatogonia), was also investigated. Enhancement of marrow toxicity could be demonstrated only at CCNU doses > 12 5 mg/kg, so that at lower CCNU doses there was a therapeutic gain equal to the tumour enhancement ratio. The spermatogonia effect, however, showed enhancement by MISO similar to that seen in the tumours at all CCNU doses up to 20 mg/kg.

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“…In the mouse we know, from the interval between treatment and a given mating, the stage of maturation that the sperm used in that mating had reached at the time of treatment. This is because the time-table of spermatogenesis has been established by Oakberg (1956) and the time taken for the passage of sperm through epididymis and vas deferens has been estimated by Sirlin and Edwards (1957). Thus, one can assess the mutagenic sensitivity of the various stages of maturation.…”

Section: Introductionmentioning

confidence: 99%

The sensitivity of the male germ cells of Drosophila to methyl methanesulphonate

Bateman

Chandley

1964

Heredity

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Duration of spermatogenesis in the mouse and timing of stages of the cycle of the seminiferous epithelium

Cited by 892 publications

References 8 publications

Recovery of a low mutant frequency after ionizing radiation-induced mutagenesis during spermatogenesis

Recovery of a low mutant frequency after ionizing radiation-induced mutagenesis during spermatogenesis

Enhancement of CCNU cytotoxicity by misonidazole: possible therapeutic gain

The sensitivity of the male germ cells of Drosophila to methyl methanesulphonate

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