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Updated: Aug 15, 2025

An In Vivo Method to Study Mouse Blood-Testis Barrier Integrity
Published on: December 2, 2018
Effect of di(n-butyl) phthalate on the blood-testis barrier during puberty onset
Reneilwe A Molele1, Musa Zakariah2,3, Mohammed I A Ibrahim4,5
1Department of Production Animal Studies, Faculty of Veterinary Science, University of Pretoria, Pretoria, South Africa.
Abstract:
Di(n-butyl) phthalate (DBP) is considered a substance of serious concern because of its reproductive toxicity and endocrine-disrupting properties. Exposure to DBP causes morphological and functional changes in the male reproductive system of birds and mammals. However, there are no detailed reports on the effects of DBP on the Sertoli cell and junctional complexes of the blood-testis barrier (BTB) in birds. The present study investigated dose-related ultrastructural changes in Sertoli cells and junctional complexes of the BTB in adult Japanese quail (Coturnix coturnix japonica) exposed to DBP prior to puberty. A total of 25 Japanese quail were used for the study. Exposure to DBP doses of 50, 200 and 400 mg DBP/kg/d caused dose-related ultrastructural changes in junctional complexes including dilation and separation, while disruption of cytoplasmic membranes and mitochondria was observed in Sertoli cells. There was a significant difference in the sum of vacuoles, vacuole diameter, nuclear width, nuclear length, nuclear area, sum of damaged spherical mitochondria, width of elongated mitochondria and the sum of damaged elongated mitochondria among the five treatment groups (p ˂ 0.05). Prepubertal exposure to DBP at doses of 50, 200 and 400 mg DBP/kg/d for 30 days led to adverse effects in the adult male Japanese quail reproductive system by inducing structural changes in the Sertoli cells and junctional complexes. Such changes might disrupt the BTB and potentially interfere with spermatogenesis. Results indicated that the Sertoli cell is sensitive to DBP exposure and might be an important cellular target for DBP-induced testicular toxicity.
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