TY - JOUR
T1 - The effects of prenatal and lactational bisphenol A and/or di(2-ethylhexyl) phthalate exposure on female reproductive system
AU - Ozkemahli, Gizem
AU - Balci Ozyurt, Aylin
AU - Erkekoglu, Pinar
AU - Zeybek, Naciye Dilara
AU - Yersal, Nilgun
AU - Kocer-Gumusel, Belma
N1 - Publisher Copyright:
© 2022 Informa UK Limited, trading as Taylor & Francis Group.
PY - 2022
Y1 - 2022
N2 - Bisphenol A (BPA) and di(2-ethylhexyl) phthalate (DEHP) are endocrine disrupting chemicals (EDCs) that are abundantly used in polyvinyl chloride plastics, polycarbonates and epoxy resins. Prenatal and early postnatal exposures to EDCs are suggested to be more critical. Such exposures can lead to reprotoxic effects, hormonal and metabolic consequences in adulthood. Moreover, combined exposure to different EDCs can lead to more serious adverse effects, some of which cannot be predicted by examining their individual toxicity profiles. This study aimed to evaluate effects of single and combined prenatal and lactational exposures to BPA and/or DEHP on female reproductive hormones and ovarian follicle development. Pregnant Sprague-Dawley rats were divided randomly to four groups (n = 3/group): Control (received vehicle only); DEHP (30 mg/kg/day); BPA (50 mg/kg/day) and BPA + DEHP (30 mg/kg/day DEHP; 50 mg/kg/day BPA) through 6–21 gestational days and lactation by intra-gastric lavage. Female offspring (n = 6/group) were fed until the end of twelfth postnatal week and then euthanized. Reproductive hormones, ovarian follicle numbers and ovarian development were determined. Plasma testosterone and estradiol levels of BPA and BPA + DEHP groups were significantly lower than control. In BPA group, the number of tertiary ovarian follicles decreased significantly compared to control. In the combined exposure group, the number of corpus luteum (29%), as well as the number of primordial follicles (36%), showed marked decreases compared to control group. It can be suggested that early life exposure to BPA and DEHP may cause late life adverse effects in female reproductive system, especially after combined exposure.
AB - Bisphenol A (BPA) and di(2-ethylhexyl) phthalate (DEHP) are endocrine disrupting chemicals (EDCs) that are abundantly used in polyvinyl chloride plastics, polycarbonates and epoxy resins. Prenatal and early postnatal exposures to EDCs are suggested to be more critical. Such exposures can lead to reprotoxic effects, hormonal and metabolic consequences in adulthood. Moreover, combined exposure to different EDCs can lead to more serious adverse effects, some of which cannot be predicted by examining their individual toxicity profiles. This study aimed to evaluate effects of single and combined prenatal and lactational exposures to BPA and/or DEHP on female reproductive hormones and ovarian follicle development. Pregnant Sprague-Dawley rats were divided randomly to four groups (n = 3/group): Control (received vehicle only); DEHP (30 mg/kg/day); BPA (50 mg/kg/day) and BPA + DEHP (30 mg/kg/day DEHP; 50 mg/kg/day BPA) through 6–21 gestational days and lactation by intra-gastric lavage. Female offspring (n = 6/group) were fed until the end of twelfth postnatal week and then euthanized. Reproductive hormones, ovarian follicle numbers and ovarian development were determined. Plasma testosterone and estradiol levels of BPA and BPA + DEHP groups were significantly lower than control. In BPA group, the number of tertiary ovarian follicles decreased significantly compared to control. In the combined exposure group, the number of corpus luteum (29%), as well as the number of primordial follicles (36%), showed marked decreases compared to control group. It can be suggested that early life exposure to BPA and DEHP may cause late life adverse effects in female reproductive system, especially after combined exposure.
KW - Endocrine disruptors
KW - bisphenol A
KW - combined exposure
KW - female reproductive system
KW - phthalate
UR - http://www.scopus.com/inward/record.url?scp=85129194635&partnerID=8YFLogxK
U2 - 10.1080/15376516.2022.2057265
DO - 10.1080/15376516.2022.2057265
M3 - Article
C2 - 35321620
AN - SCOPUS:85129194635
SN - 1537-6516
VL - 32
SP - 597
EP - 605
JO - Toxicology Mechanisms and Methods
JF - Toxicology Mechanisms and Methods
IS - 8
ER -