Exposure of young rats to high estrogen doses leads to degeneration of elongated spermatids

• Published in: Tissue & cell 2008-02, Vol.40 (1), p.31-42
• Main Authors: Pinto, M.E, Vilamaior, P.S.L, Taboga, S.R, Góes, R.M
• Format: Article
• Language: English
• Subjects: Advanced Basic Science; Animals; Apoptosis; Estrogens; Estrogens - administration & dosage; Estrogens - toxicity; Germ Cells - drug effects; Germ Cells - metabolism; Male; Rats; Rats, Wistar; Seminiferous Epithelium - cytology; Seminiferous Epithelium - metabolism; Spermatids - drug effects; Spermatids - physiology; Spermatids - ultrastructure; Spermatogenesis; Testis
• ISSN: 0040-8166; 1532-3072
• DOI: 10.1016/j.tice.2007.09.002

Abstract Single high doses of estrogen (35 mg/kg body weight) were administered to young rats aiming to exacerbate its effects on germ cell populations. The short-term (1 week) and medium-term (7 weeks) consequences of this estrogenic treatment (ET) on the testis were evaluated using light and electron microscopies, quantitative methods and TUNEL reaction. Short-term ET led to 50% atrophy of the testis, however, in the medium term the gonado-somatic index was recovered. No histopathological alterations were found at seminiferous epithelium except for short-term severe degeneration of elongated spermatids (EL) and low frequency of these cells in both time intervals. Two morphologically distinct patterns of degeneration were observed: (1) clusters of EL which were TUNEL-negative and exhibited bizarre appearance and nuclear fragmentation, (2) isolated apoptotic EL within the cytoplasm of Sertoli cells (SC). Both degenerative phenomena were more frequent in stages III–VIII of seminiferous cycle, whereas at stages I and II only coiling of flagellum was observed. One week after ET, small amounts of EL were detected in stages IX–XII, suggesting spermiation failure. Signs of functional SC damage such as an accumulation of myelin-like inclusions in their cytoplasm were observed in the short but not medium-term. However, the apoptotic rates still remained five times higher and the number of elongated spermatids was three-fold lower. Our data indicate that exposure to a high dose of estrogen around puberty has stage-specific effects on the testis and causes massive degeneration of elongated spermatids.