Abstract
Di (2-ethylhexyl) phthalate (DEHP), an estrogen-like compound that is a ubiquitous environmental contaminant, has been reported to adversely affect human and mammalian reproduction. Many studies have found that exposure to DEHP during pregnancy perturbs female germ cell meiosis and is detrimental to oogenesis. Previous studies have demonstrated that melatonin (MLT) is beneficial to reproductive endocrinology, oogenesis, and embryonic development as the ability to antioxidative and antiapoptotic. However, whether the meiotic defect of germ cells exposed to DEHP could be rescued by MLT is not clear. Here, we cultured 12.5 days post coitum (dpc) fetal mouse ovaries for 6 days, exposed them to 100 μM DEHP with or without 1 μM MLT in vitro.. The results showed that DEHP exposure induced the abnormal formation of DNA double-strand breaks (DSBs), and inhibited the repair of DSBs during meiotic recombination. In addition, we found defective oocytes were prone to undergo apoptosis. Notably, this defect could be remarkably ameliorated by the addition of MLT via a reduction of the levels of reactive oxygen species and an inhibition of apoptosis. In conclusion, our data revealed that MLT had a protective action against the meiotic deterioration of fetal oocytes induced by DEHP in the mouse in vitro.
Highlights
Mammalian reproduction is critical for perpetuating and diversifying the genetic information across generations [1, 2], and normal germ cell development is critical for the genetic stability of a species [3]
We found that Di (2‐ethylhexyl) phthalate (DEHP) exposure during gestation perturbs female germ cell meiosis and primordial follicle assembly [9, 20]
DEHP exposure reduced the mRNA expressions of Sycp3, but markedly increased the mRNA levels of the DNA damage-related gene Trp53 when compared with that of the control group (Figure 1C; P < 0.05 or P < 0.01)
Summary
Mammalian reproduction is critical for perpetuating and diversifying the genetic information across generations [1, 2], and normal germ cell development is critical for the genetic stability of a species [3]. Germ cells begin entry into meiosis during the fetal stage, which is fundamental to the production of viable of a sexually reproducing species [4]. During the first meiosis prophase (MPI), DNA double-strand breaks (DSBs) sever entire chromosomes and pose a severe hazard to genomic integrity because of chromosomal fragment loss or chromosomal rearrangements [5]. These DSBs can be repaired by homologous recombination (HR) dependent mechanisms, and establish links between unassociated homologs [6, 7]. A recent study has reported that Di (2-ethylhexyl) phthalate (DEHP) exposure impairs MPI and DNA damage repair in female fetal mouse germ cells in vitro, and acts through multiple pathways including DNA damage and apoptosis pathways [9]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
