Biol Reprod 2009 SSR Annual Meeting Abstracts
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Biology of Reproduction 63, 1245-1252 (2000)
© 2000 Society for the Study of Reproduction, Inc.


Regular Article

Ultrastructural Evaluation of Oocytes During Atresia in Rat Ovarian Follicles1

P.J. Devine2,,a, C.M. Payneb,d, M.K. McCuskeyc, and P.B. Hoyera

a Departments of Physiology, b Microbiology and Immunology, c Cell Biology and Anatomy, and d Arizona Cancer Center, The University of Arizona, Tucson, Arizona 85724

ABSTRACT

Mammalian females are born with a finite number of ovarian oocytes, the vast majority of which ultimately undergo degeneration by atresia. The overall process of ovarian follicular atresia has been morphologically well described only in large antral follicles. Additionally, little attention has been focused on ultrastructural changes in the oocyte. Furthermore, most such morphological studies were performed prior to identification of apoptosis as a mechanism of physiological cell death. Therefore, the purpose of this study was to use electron microscopy to compare the process of atretic oocyte degradation in ovarian follicles of female Fischer 344 rats (38 days old) with ultrastructural characteristics of apoptosis. Examination of ovarian follicles revealed that nucleolar segregation, cytoplasmic or nuclear condensation, apoptotic body formation, and chromatin margination along the nuclear membrane are never observed in atretic oocytes during the degenerative process. Instead, early morphological changes in atretic oocytes include retraction of granulosa cell- and oocyte-derived microvilli and condensation of mitochondria and loss of cristae. These occurrences coincide with initiation of granulosa cell apoptosis. After most granulosa cells are lost, more severe changes occur, including segmentation of the oocyte and cytoplasmic vacuolization as atresia progresses. Thus, these results suggest that, during atresia, oocytes are removed by physiological oocyte cell death, a method that does not involve classically described apoptosis.

FOOTNOTES

First decision: 26 April 2000.

1 This research was funded by the Arizona Disease Control Research Council, NIH grants ES98979 and Toxicology Center grant ES06694.

2 Correspondence: Patrick J. Devine, 1501 North Campbell Ave., Department of Physiology, The University of Arizona, P.O. Box 245051, Tucson, AZ 85724-5051. FAX: 520 626 2382; pdevine{at}u.arizona.edu




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