Histopathologic, apoptotic and autophagic, effects of prenatal bisphenol A and/or di(2-ethylhexyl) phthalate exposure on prepubertal rat testis

Balci A., ÖZKEMAHLI K. G., ERKEKOĞLU Ü. P., ZEYBEK N. D., YERSAL N., Kocer-Gumusel B.

Environmental Science and Pollution Research, vol.27, no.16, pp.20104-20116, 2020 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 27 Issue: 16
  • Publication Date: 2020
  • Doi Number: 10.1007/s11356-020-08274-6
  • Journal Name: Environmental Science and Pollution Research
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus, IBZ Online, ABI/INFORM, Aerospace Database, Agricultural & Environmental Science Database, Aqualine, Aquatic Science & Fisheries Abstracts (ASFA), BIOSIS, CAB Abstracts, EMBASE, Environment Index, Geobase, MEDLINE, Pollution Abstracts, Veterinary Science Database, Civil Engineering Abstracts
  • Page Numbers: pp.20104-20116
  • Keywords: Phthalate, Bisphenol A, Male reproductive system, Prenatal exposure, Autophagy, Apoptosis, MATERNAL EXPOSURE, IN-UTERO, DIETHYLHEXYL PHTHALATE, DEVELOPMENTAL ORIGINS, DEHP, HEALTH, HORMONES, BPA, EXPRESSION, LACTATION
  • Lokman Hekim University Affiliated: Yes


© 2020, Springer-Verlag GmbH Germany, part of Springer Nature.Bisphenol A (BPA) and di(2-ethylhexyl) phthalate (DEHP) are endocrine-disrupting chemicals (EDCs) used in a wide variety of industrial products as plasticizers. Exposure to EDCs, particularly in mixtures, in prenatal and early postnatal periods may lead to unwanted effects and can cause both developmental and reproductive problems. In this study, we aimed to determine the individual and combined effects of prenatal and lactational exposure to BPA and/or DEHP on testicular histology, apoptosis, and autophagic proteins. Pregnant Sprague-Dawley rats (n = 3) were divided into four groups (control, BPA (50 mg/kg/day), DEHP (30 mg/kg/day), and BPA (50 mg/kg/day) + DEHP (30 mg/kg/day)) and dosed by oral gavage during pregnancy and lactation. The male offspring (n = 6) from each group were chosen randomly, and their testicular examinations were performed on the twelfth week. The results showed that fetal and neonatal exposure to BPA and DEHP could lead to significant testicular histopathological alterations and cause increases in apoptosis markers (as evidenced by increases in caspase 3 and caspase 8 levels; increased TUNEL-positive spermatogonia and TUNEL-positive testicular apoptotic cells) and autophagic proteins (as evidenced by increased LC3 and Beclin levels and decreased p62 levels) in testicular tissue. We can suggest that EDCs cause more dramatic changes in both testicular structure and cell death when there is combined exposure.