Intrauterine exposure to diethylhexyl phthalate disrupts gap junctions in the fetal rat testis

• Published in: Current research in toxicology 2020-06, Vol.1, p.5-11
• Main Authors: Di Lorenzo, Mariana, Winge, Sofia Boeg, Svingen, Terje, De Falco, Maria, Boberg, Julie
• Format: Article
• Language: English
• Subjects: CX43; DEHP; Endocrine disrupting chemicals; Gap junctions; Phthalates; Testis
• ISSN: 2666-027X; 2666-027X
• DOI: 10.1016/j.crtox.2020.02.002

Fetal exposure to certain phthalate esters can disrupt testis development in rodents and lead to male reproductive disorders, but with a causal link less certain in humans. Di(2-ethylhexyl) phthalate (DEHP) is one of the most common phthalates found in the environment and in rodents it is known to induce serious testis toxicity, as well as male reproductive disorders including cryptorchidism, hypospadias, impaired spermatogenesis and reduced fertility. In this study, we show that perinatal DEHP exposure disrupts gap junction localization in fetal and postnatal rat testis and correlate these findings to morphological changes. The protein Connexin 43 (CX43), normally expressed strongly in testicular gap junctions, was markedly downregulated in Leydig cells of DEHP-exposed fetal testes. In the postnatal testes, CX43 expression was recovered in the DEHP-exposed animals, even though Leydig cell clusters and malformed cords with intratubular Leydig cells were still present. [Display omitted] •DEHP disrupts gap junction localization in fetal and postnatal rat testis.•DEHP exposure reduces Cx43-positive gap junctions in Leydig cell clusters in fetal rat testis.•Leydig cell gap junctions recover in postnatal testis after early life DEHP exposure.