Literature DB >> 426311

Degeneration of mouse oocytes in response to polycyclic aromatic hydrocarbons.

B J Gulyas, D R Mattison.   

Abstract

Destruction of mouse oocytes in primordial and small primary follicles in response to treatment with 3-methylcholanthrene (MC) was studied at the ultrastructural level. Four-week old C57Bl/6N (B6) strain mice received a single injection of 80 mg/Kg MC in corn oil intraperitoneally. Controls received only corn oil. Ovaries from animals were prepared for light and electron microscopic examination at specified intervals after treatment. The number of primordial follicles remained constant in control animals. In contrast, their number decreased significantly (P less than 0.01) by three days, and they were depleted by seven days after MC treatment. Subtle degenerative modifications were noted in the ooplasm of primordial follicles two days after treatment. These changes consisted of vesiculation of mitochondrial cristae, increased electron density of the mitochondrial matrix, myelin structures in lipid droplets and in mitochondria. More advanced stages of degeneration of primordial follicles were characterized by further vesiculation or disappearance of mitochondrial cristae, chromatin clumping, and increased density of the ooplasm. Small primary follicles had undergone similar initial degeneration as primordial follicles. In more advanced stages of degeneration nuclear and cytoplasmic contents condensed, endoplasmic reticulum, Golgi complex and mitochondria swelled, small vesicles and multivesicular bodies appeared. In the most advanced stages of degeneration of small primary follicles it appeared that small portions of the oocyte were engulfed by the surrounding follicular cells. It is concluded that exposure of B6 mice to a single dose of MC results in atresia of oocytes in primordial and small primary follicles. Ultrastructurally, these degenerating oocytes of treated mice looked much like the spontaneously atretic oocytes in untreated animals.

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Year:  1979        PMID: 426311     DOI: 10.1002/ar.1091930409

Source DB:  PubMed          Journal:  Anat Rec        ISSN: 0003-276X


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