Involvement of Bcl-2 Family Genes and Fas Signaling System in Primary and Secondary Male Germ Cell Apoptosis Induced by 2-Bromopropane in Rat

Yu, Xiaozhong; Kubota, Hisayo; Wang, Rui-Sheng; Saegusa, Junzo; Ogawa, Yasutake; Ichihara, Gaku; Takeuchi, Yasuhiro; Hisanaga, Naomi

doi:10.1006/taap.2001.9187

Cited by 51 publications

(38 citation statements)

References 49 publications

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“…In case of DES treatment, Bax protein translocation to mitochondria occurred after caspase-8 was activated. A role for Bax has been predicted in germ cell apoptosis using different models, but predictions of involvement of Bax have largely been made based on cellular localization (17,52) or from Western blots of whole testis extracts (53). Using purified spermatogenic cells, our study clearly demonstrates that there is a translocation of Bax from the cytosol to the mitochondria resulting in the release of cytochrome c. In certain cell types, cytochrome c release is accompanied by a fall in mitochondrial potential (54) and our studies show that in spermatogenic cells the ⌬ m fall is preceded by a transient increase in reactive oxygen species (data not shown) and followed by a fall in ATP levels.…”

Section: Discussionmentioning

confidence: 99%

Diethylstilbestrol Induces Rat Spermatogenic Cell Apoptosis in Vivo through Increased Expression of Spermatogenic Cell Fas/FasL System

Nair

Shaha

2003

Journal of Biological Chemistry

105

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The significant role that estrogens play in spermatogenesis has opened up an exciting area of research in male reproductive biology. The realization that estrogens are essential for proper maintenance of spermatogenesis, as well as growing evidence pointing to the deleterious effects of estrogen-like chemicals on male reproductive health, has made it imperative to dissect the role estrogens play in the male. Using a model estrogen, diethylstilbestrol (DES), to induce spermatogenic cell apoptosis in vivo in the male rat, we provide a new insight into an estrogen-dependent regulation of the Fas-FasL system specifically in spermatogenic cells. We show a distinct increase in Fas-FasL expression in spermatogenic cells upon exposure to diethylstilbestrol. This increase is confined to the spermatid population, which correlates with increased apoptosis seen in the haploid cells. Testosterone supplementation is able to prevent DES-induced Fas-FasL up-regulation and apoptosis in the spermatogenic cells. DES-induced germ cell apoptosis does not occur in Fas-deficient lpr mice. One other important finding is that spermatogenic cells are type II cells, as the increase in Fas-FasL expression in the spermatogenic cells is followed by the cleavage of caspase-8 to its active form, following which Bax translocates to the mitochondria and precipitates the release of cytochrome c that is accompanied by a drop in mitochondrial potential. Subsequent to this, activation of caspase-9 occurs that in turn activates caspase-3 leading to the cleavage of poly(ADP-ribose) polymerase. Taken together, the data indicate that estrogen-like chemicals can precipitate apoptotic death in spermatogenic cells by increasing the expression of spermatogenic cell FasFasL, thus initiating apoptosis in the same lineage of cells through the activation of the apoptotic pathway chosen by type II cells.

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Section: Discussionmentioning

confidence: 99%

Diethylstilbestrol Induces Rat Spermatogenic Cell Apoptosis in Vivo through Increased Expression of Spermatogenic Cell Fas/FasL System

Nair

Shaha

2003

Journal of Biological Chemistry

105

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“…But it was not investigated in previous studies. TUNEL staining of DNA fragments is routinely used for the detection of apoptotic cells in various tissues, and it is also a sensitive and valid method for identification of apoptotic cells within the seminiferous epithelium (Yu et al 2001).…”

Section: Introductionmentioning

confidence: 99%

Hypobaric hypoxia causes deleterious effects on spermatogenesis in rats

Liao¹,

Cai²,

Chen³

et al. 2010

Reproduction

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The study was conducted to explore the effects of hypobaric hypoxia on spermatogenesis in rats. Adult male Wistar rats were randomly divided into four groups: three hypoxia-exposed groups and one normoxic control group. Rats in the normoxic control group were raised at an altitude of 300 m, while rats in the 5-, 15-, and 30-day hypoxic groups were raised in a hypobaric chamber simulating a high altitude of 5000 m for 5, 15, and 30 days respectively. Flow cytometry was used to detect the DNA content of testicular spermatogenic cells in rats. The apoptosis of germ cells in testis was analyzed by using TUNEL assay. Spermatogenesis was also evaluated by morphology. Flow cytometry analysis revealed that 5-30 days of hypobaric hypoxia exposure significantly reduced the percentage of tetraploid cell population in rat testis. After rats were exposed to hypobaric hypoxia for 30 days, the ratio of haploid and diploid cell populations in testis reduced significantly. Seminiferous tubules with apoptotic germ cell increased after exposure to hypoxia. Most apoptotic germ cells were spermatogonia and spermatocytes. Hypoxia also caused decrease of cellularity of seminiferous epithelium, degeneration and sloughing of seminiferous epithelial cells occasionally. The data suggest that hypobaric hypoxia inhibits the spermatogenesis in rats. Decrease of tetraploid spermatogenic cells (primary spermatocytes) induced by hypoxia is an important approach to suppress spermatogenesis. The apoptosis of primary spermatocytes and spermatogonia may contribute to the loss of tetraploid cell populations.

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“…Example of direct intrinsic germ cell apoptosis include hormone deprivation (see companion manuscript by Weinbauer, this issue), gamma irradiation, 2-bromopropane induced germ cell apoptosis. 4,49 Evidence for the functional participation of regulators of the intrinsic signaling system in spermatogenesis comes from several transgenic and gene knockout mice (reviewed in 3 ). From these mouse studies, it is clear that the overexpression or inhibition of either proapoptotic or antiapoptotic family members results in the loss of germ cells by apoptosis.…”

Section: Intrinsic Signalingmentioning

confidence: 99%

Implications of Sertoli cell induced germ cell apoptosis to testicular pathology

Murphy

Richburg

2014

Spermatogenesis

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Involvement of Bcl-2 Family Genes and Fas Signaling System in Primary and Secondary Male Germ Cell Apoptosis Induced by 2-Bromopropane in Rat

Cited by 51 publications

References 49 publications

Diethylstilbestrol Induces Rat Spermatogenic Cell Apoptosis in Vivo through Increased Expression of Spermatogenic Cell Fas/FasL System

Diethylstilbestrol Induces Rat Spermatogenic Cell Apoptosis in Vivo through Increased Expression of Spermatogenic Cell Fas/FasL System

Hypobaric hypoxia causes deleterious effects on spermatogenesis in rats

Implications of Sertoli cell induced germ cell apoptosis to testicular pathology

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