A Method for Quantifying Synchrony in Testes of Rats Treated with Vitamin A Deprivation and Readministration1

Beek, M. E. A. B. van; Meistrich, Marvin L.

doi:10.1095/biolreprod42.3.424

Cited by 40 publications

(23 citation statements)

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“…Van Beek and Meistrich (6) introduced a synchronization factor to quantify the degree of synchronization. After 49 days of RA injections twice weekly, we could calculate from our data a synchronization factor of 1.5-2.3, in contrast to values of 2.4-3.1 found after 36 days of retinol replacement (6). This together with the fact that not all round spermatids are able to elongate during RA injection twice weekly suggests that even higher or more frequent doses of RA are needed to obtain an optimal support of the spermatogenic process such as that after retinol replacement.…”

Section: Discussioncontrasting

confidence: 88%

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Retinoic Acid Is Able to Reinitiate Spermatogenesis in Vitamin A-Deficient Rats and High Replicate Doses Support the Full Development of Spermatogenic Cells

Pelt¹,

Rooij²

1991

Endocrinology

193

102

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The effect of various doses of retinoic acid (RA) on the seminiferous epithelium in vitamin A-deficient rats has been studied. Although it was generally thought that RA was not able to reinitiate spermatogenesis in vitamin A-deficient rats, one injection of 5 mg RA strongly stimulated the proliferative activity of A-spermatogonia within 24 h, as evidenced by a 7-fold increase in the number of bromodeoxyuridine-labeled A-spermatogonia. Ten days after RA administration, B-spermatogonia or preleptotene spermatocytes were seen in most of the seminiferous tubules. After 15 days, zygotene spermatocytes were present. Hence, RA is able to induce a massive and synchronized development of A-spermatogonia into spermatocytes. When RA was given once, combined with a RA-containing diet, only few of the zygotene spermatocytes present on day 15 were able to develop into pachytene spermatocytes, which did not develop into spermatids. In subsequent epithelial cycles new B-spermatogonia and spermatocytes were formed, although in lower numbers than during the first cycle after RA injection. When RA was given once a week, the formation of B-spermatogonia and preleptotene spermatocytes continued at a higher level. Also, more pachytene spermatocytes were formed, some of which were able to develop into spermatids. Finally, when RA was injected twice a week, even more pachytene spermatocytes and round spermatids were found after 36 days, and after 49 days elongated spermatids were found in all animals. It is concluded that RA, similar to retinol, is able to induce synchronous proliferation and differentiation of A-spermatogonia. When repeated injections are given, RA is able to support the full development of spermatogenic cells into elongated spermatids.

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Section: Discussioncontrasting

confidence: 88%

“…Ultimately, the seminiferous tubules of vitamin A-deficient rats only contain Sertoli cells, A-spermatogonia, and some spermatocytes (3,4). Administration of retinol acetate causes a massive and synchronized reinitiation of spermatogenesis in vitamin A-deficient rats (4)(5)(6).…”

mentioning

confidence: 99%

Retinoic Acid Is Able to Reinitiate Spermatogenesis in Vitamin A-Deficient Rats and High Replicate Doses Support the Full Development of Spermatogenic Cells

Pelt¹,

Rooij²

1991

Endocrinology

193

102

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“…The synchrony factor for each sample was determined using the methods described by Siiteri et al [27] and Van Beek and Meistrich [28]. This value is a numerical representation of the degree of synchrony present within each sample and allows for comparison between control and conditional knockout samples.…”

Section: Staging Analysis Of Synchronized Tissuementioning

confidence: 99%

“…Testes from 90-dpp Cyp26a1/b1 Flox/þ;Creþ controls and Cyp26a1/b1 Flox/Flox;Creþ knockout mice were immunostained with STRA8, the testis tubules were staged according to Russell et al [26], and a synchrony factor was calculated [27,28], allowing for quantitative comparison of spermatogenic synchrony between samples. Neither germ cellnor Sertoli cell-specific elimination of CYP26A1 and CYP26B1 activity resulted in a change in spermatogenic cycle FIG.…”

Section: Asynchronous Spermatogenesis Occurs In Male Mice Lacking Cypmentioning

confidence: 99%

CYP26 Enzymes Are Necessary Within the Postnatal Seminiferous Epithelium for Normal Murine Spermatogenesis1

Hogarth

Evans

Onken

et al. 2015

Biology of Reproduction

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The active metabolite of vitamin A, retinoic acid (RA), is known to be essential for spermatogenesis. Changes to RA levels within the seminiferous epithelium can alter the development of male germ cells, including blocking their differentiation completely. Excess RA has been shown to cause germ cell death in both neonatal and adult animals, yet the cells capable of degrading RA within the testis have yet to be investigated. One previous study alluded to a requirement for one of the RA degrading enzymes, CYP26B1, in Sertoli cells but no data exist to determine whether germ cells possess the ability to degrade RA. To bridge this gap, the roles of CYP26A1 and CYP26B1 within the seminiferous epithelium were investigated by creating single and dual conditional knockouts of these enzymes in either Sertoli or germ cells. Analysis of these knockout models revealed that deletion of both Cyp26a1 and Cyp26b1 in either cell type resulted in increased vacuolization within the seminiferous tubules, delayed spermatid release, and an increase in the number of STRA8-positive spermatogonia, but spermatozoa were still produced and the animals were found to be fertile. However, elimination of CYP26B1 activity within both germ and Sertoli cells resulted in severe male subfertility, with a loss of advanced germ cells from the seminiferous epithelium. These data indicate that CYP26 activity within either Sertoli or germ cells is essential for the normal progression of spermatogenesis and that its loss can result in reduced male fertility.

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“…The first indication that RA drives spermatogonial differentiation was deduced from studies examining testes of VAD rodents (Huang and Hembree 1979;Ismail et al 1990;Mitranond et al 1979;Morales and Griswold 1987;Van Beek and Meistrich 1990;van Pelt and de Rooij 1990;van Pelt et al 1995;Wang and Kim 1993). The placement of wild-type adult rodents with normal spermatogenesis on a VAD diet resulted in the sloughing of advanced germ cells into the lumen of the testis tubules and loss of fertility in approximately 9-11 weeks.…”

Section: Vitamin a Deficiencymentioning

confidence: 99%

Germ Cell Commitment to Oogenic Versus Spermatogenic Pathway: The Role of Retinoic Acid

Agrimson

Hogarth

2016

Results and Problems in Cell Differentiation

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The core of the decision to commit to either oogenesis or spermatogenesis lies in the timing of meiotic entry. Primordial germ cells within the fetal ovary become committed to the female pathway prior to birth and enter meiosis during embryonic development. In the fetal testis, however, the germ cells are protected from this signal before birth and instead receive this trigger postnatally. There is a growing body of evidence to indicate that RA is the meiosis-inducing factor in both sexes, with the gender-specific timing of meiotic entry controlled via degradation of this molecule only within the fetal testis. This chapter will review our current understanding of how RA controls germ cell fate in both the embryonic ovary and postnatal testis, highlighting the key studies that have led to the hypothesis that RA can drive the commitment to meiosis in both sexes and discussing the current debate over whether RA truly is the meiosis-inducing factor in the fetal ovary.

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A Method for Quantifying Synchrony in Testes of Rats Treated with Vitamin A Deprivation and Readministration1

Cited by 40 publications

References 0 publications

Retinoic Acid Is Able to Reinitiate Spermatogenesis in Vitamin A-Deficient Rats and High Replicate Doses Support the Full Development of Spermatogenic Cells

Retinoic Acid Is Able to Reinitiate Spermatogenesis in Vitamin A-Deficient Rats and High Replicate Doses Support the Full Development of Spermatogenic Cells

CYP26 Enzymes Are Necessary Within the Postnatal Seminiferous Epithelium for Normal Murine Spermatogenesis1

Germ Cell Commitment to Oogenic Versus Spermatogenic Pathway: The Role of Retinoic Acid

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