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

Mariana Di Lorenzo, Sofia Boeg Winge, Terje Svingen, Maria De Falco, Julie Boberg*

*Corresponding author for this work

Research output: Contribution to journalJournal articleResearchpeer-review

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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.
Original languageEnglish
JournalCurrent Research in Toxicology
Pages (from-to)5-11
Publication statusPublished - 2020


  • Phthalates
  • DEHP
  • Testis
  • Endocrine disrupting chemicals
  • Gap junction
  • CX43


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