Histopathologic, apoptotic and autophagic, effects of prenatal bisphenol A and/or di(2-ethylhexyl) phthalate exposure on prepubertal rat testis
| Autor: | Belma Kocer-Gumusel, Aylin Balci, Pinar Erkekoglu, Naciye Dilara Zeybek, Nilgün Yersal, Gizem Özkemahlı |
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| Přispěvatelé: | EBYÜ, Eczacılık Fakültesi |
| Jazyk: | angličtina |
| Rok vydání: | 2020 |
| Předmět: |
Male
Programmed cell death endocrine system Offspring Health Toxicology and Mutagenesis Phthalic Acids Caspase 3 Apoptosis 010501 environmental sciences 01 natural sciences Rats Sprague-Dawley Andrology chemistry.chemical_compound Bisphenol A Phenols Plasticizers Pregnancy Diethylhexyl Phthalate Lactation Prenatal exposure Testis medicine Autophagy Animals Environmental Chemistry Benzhydryl Compounds 0105 earth and related environmental sciences Fetus business.industry urogenital system Phthalate General Medicine medicine.disease Pollution Rats medicine.anatomical_structure chemistry Male reproductive system s Phthalate Prenatal Exposure Delayed Effects Female business |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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