Biochemical and histological validation of a model to study follicular atresia in rats.

Abstract

A model system to study the biochemical mechanism of follicular atresia in rats [Dhanasekaran et al. 1983] was characterized using histological and biochemical correlates. PMSG and PMSG antiserum (a/s) was used to induce the follicular growth and atresia of preovulatory follicles. Ovarian histology during these PMSG and PMSG a/s - treatment periods was recorded under a light microscope. An analysis of lysosomal enzyme cathepsin-D activity of granulosa cells (GC) from similarly treated ovaries showed that there was a reduction in cathepsin-D activity during the histologically observable follicular growth; and there was an increase in cathepsin-D activity during atresia. The increase in cathepsin-D activity also showed an inverse correlation with the general anabolic activity of the GC as demonstrated here, by a reduction in 3H-leucine incorporation activity. An analysis of other gonadotropin-responsive cells for the presence of such hormone sensitive lysosomal machinery, only corpora lutea (CL) and GC showed in the cathepsin-D activity upon treatment with 15 IU of PMSG. The results suggests the existence of a common gonadotropin regulated lysosomal machinery in cells endowed with a degenerative pathway of "programmed cell death". More importantly the results establish the validity of using lysosomal enzyme cathepsin-D as a biochemical marker, for hitherto morphologically and endocrinologically studied cellular degenerative process of follicular atresia.