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Atresia and Apoptosis in Pre- and Postovulatory Follicles of Sharptooth Catfish (Clarias gariepinus, Burchell, 1822)

Atresia and Apoptosis in Pre- and Postovulatory Follicles of Sharptooth Catfish (Clarias gariepinus, Burchell, 1822)

Şehriban Çek Yalnız 1,* and Erdal Yilmaz2

1Faculty of Marine Sciences and Technology, Iskenderun Technical University, İskenderun 31200, Hatay, Turkey
2Faculty of Veterinary Sciences, University of Erciyes, 38039 Melikgazi, Kayseri, Turkey

*      Corresponding author:



Ovarian follicular atresia and postovulatory regression in mammals is mediated by apoptosis, which is a natural occurring cause of cellular death. However, its function in fish is largely unknown. In order to discuss the possible role of apoptosis in fish ovarian follicular atresia and postovulatory regression, the pre and postovulatory follicles (POF) of the freshwater teleost, Clarias gariepinus were observed by light microscopy. The germinal vesicle and the cytoplasmic organelles of the oocyte were disintegrated. The theca of atretic mature oocytes was hypertrophied and persisted to form the interstitial cells, whereas the granulosa cells were regressed and disappeared. Erythrocytes and leukocytes were also detected at the advance stage of atresia. Apoptosis in the granulosa cells were clearly detected. The chromatin condensation against the nuclear envelope, cell shrinkage, surface blebbing and generation of apoptotic bodies by cell fragmentation were evidence of apoptosis. In pre and postovulatory follicles, karyorhexis and the budding phenomena were clearly detected. Karyorhexis and budding phenomena were also the sing of apoptosis. Atresia was also clearly detected in pre and postovulatory follicles. The detection of karyorhexis, characteristic of apoptotic cells may provide a better understanding in atresia mechanism. It seems that apoptosis has a major role in the elimination of POF and atretic oocytes in the ovaries of C. gariepinus.

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Pakistan Journal of Zoology


Pakistan J. Zool., Vol. 56, Iss. 2, pp. 503-1000


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