Development of the blood–testis barrier in the mouse is delayed by neonatally administered diethylstilbestrol but not by β-estradiol 3-benzoate

Summary.  A group of newborn mice were treated with 1 µg dose⁻¹ individual⁻¹ of diethylstilbestrol (DES) on alternate days, from days 1 to 11 postnatally. Another group of mice were treated similarly with 125 ng dose⁻¹ individual⁻¹ of β-estradiol 3-benzoate (E₂B). The testes were sequentially examined up to 84 days of age using light and electron microscopy. Spermatogenic cells in the DES-treated mice differentiated normally from birth until 17 days of age, when they differentiated into pachytene spermatocytes and remained at this meiotic prophase for the next 10 days approximately. The cells then began to differentiate further, ultimately forming spermatozoa by 49 days of age. Confocal and electron microscopy showed that the blood–testis barrier did not form until 28 days of age in the DES-treated mice, and a delay in the functional maturation of this structure, as the blood–testis barrier, was confirmed by intercellular tracer experiments. The arrest of spermatogenesis at the meiotic prophase may have been attributable to the DES-induced defective formation of the blood–testis barrier. No delay of the blood–testis barrier formation was detected in the E₂B-treated mice. Thus, DES and E₂B, both of which are known as potent oestrogenic compounds, had different effects on the Sertoli cells.