Abstract
Zearalenone (ZEA) is a well-known exogenous endocrine disruptor and can lead to severe negative effects on the human and animal reproductive process. Using a follicle culture model, we have previously shown that ZEA exposure significantly affected the follicular development and antrum formation but the underlying mechanisms are not well known. Therefore, in this study, we explored the metabolomic changes of granulosa cell (GC) culture media with or without ZEA exposure. The results showed that ZEA significantly increased phosphatidylcholine or phosphatidyl ethanolamine adducts in culture medium. A comprehensive analysis with the metabolome data from follicular fluid of small and large antral follicles showed that lyso phosphatidylcholine (LPC) was accumulated during follicle growth, but was depleted by ZEA exposure. Exogenous supplement with LPC to the follicle growth media or oocyte maturation media can partly protect the defect of ZEA exposure on follicular antrum formation and oocyte maturation. Taken together, our results demonstrate that ZEA exposure hinders the follicular growth and exogenous LPC can practically protect the defect of ZEA on follicular development and oocyte maturation.
Highlights
Mycotoxin contamination affects human food and livestock feeding diet worldwide
Our results demonstrate that ZEA exposure hinders the follicular growth and exogenous lyso phosphatidylcholine (LPC) can practically protect the defect of ZEA on follicular development and oocyte maturation
In the 3-D plots, the results showed that the culture media of granulosa cell (GC) supplied with 10 μM ZEA or vehicle control had similar patterns, which were different from the blank media (Figure 2C-2E)
Summary
Zearalenone (ZEA), a nonsteroidal environmental endocrine disruptor, is produced by Fusarium fungi. ZEA has been shown to elicit various deleterious effects on the reproductive organs of human and animals [1,2,3,4,5,6,7,8,9,10,11,12,13,14,15]. The pig is the most sensitive species to the adverse effects of ZEA which induced infertility, reproductive disorders, decreased fetal viability and subsequently reduced litter size [3, 9, 13, 14]. Gestational exposure to ZEA caused early fetal death and delay in fetal development and ZEA impacted oocyte quality and follicular development, such as inhibition of oocyte maturation with abnormal spindle morphologies, disruption of actin filaments, and disturbing cortical granule extrusion [4, www.aging‐us.com
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