Zearalenone (ZEA), one of the most prevalent estrogenic mycotoxins, is mainly produced by Fusarium fungi and has been proven to affect the reproductive capacity of animals. Exposure of farm animals to ZEA is a global public health concern because of its toxicity and wide distribution in animal feeds. In vitro and in vivo experiments indicate that ZEA possesses estrogenic activity in mice, swine, Equus asinus and cattle. The precise mechanism of the reproductive toxicity of ZEA has not been established yet. This article reviews evidence on the deleterious effects of ZEA on mammalian folliculogenesis from early to final oogenesis stages. Such effects include impaired granulosa cell (GC) development and follicle steroidogenesis, reduced oocyte nest breakdown, damaged meiotic progression, poor fetal oocyte survival, accelerated primordial follicle activation and enhanced follicle atresia. These phenomena may result in reproductive and non-reproductive problems in domestic animals. In addition, emerging data indicates that ZEA may cause mRNA expression changes in the GCs. In general, E. asinus is more sensitive than swine to ZEA exposure. Finally, results of in vivo animal studies and in vitro tests are reported and discussed.

Zearalenone (ZEA) is a natural contaminant existing in food and feed products that exhibits a negative effect on domestic animals’ reproduction. Donkeys possess high economic value in China and are at risk of exposure to ZEA. However, few information is available on ZEA-induced toxicity and no report on toxicity in donkeys can be found in scientific literature. We investigated the biological effects of ZEA exposure on donkey granulosa cells (dGCs) by using RNA-seq analysis. ZEA at 10 and 30 μM were administered to GCs within 72 h of in vitro culture. ZEA at 10 μM significantly altered the tumorigenesis associated genes in dGCs. Exposure to 10 and 30 μM ZEA treatment significantly reduced mRNA expression of PTEN, TGFβ, ATM, and CDK2 genes, particularly, the ZEA treatment significantly increased the expression of PI3K and AKT genes. Furthermore, immunofluorescence, RT-qPCR, and Western blot analysis verified the gene expression of ZEA-exposed GCs. Collectively, these results demonstrated the deleterious effect of ZEA exposure on the induction of ovarian cancer related genes via the PTEN/PI3K/AKT signaling pathway in dGCs in vitro.

A full-sib intercross line (FSIL) is constructed in an outcrossing species by mating two parents and intercrossing their progeny to form a large intercross line. For given statistical power, a FSIL design requires only slightly more individuals than an F2 design derived from inbred line cross, but 6-to 10-fold fewer than a half-sib or full-sib design. Due to population-wide linkage disequilibrium, a FSIL is amenable to analysis by selective DNA pooling. In addition, a FSIL is maintained by continued intercrossing so that DNA samples and phenotypic information are accumulated across generations. Continued intercrossing also leads to map expansion and thus to increased mapping accuracy in the later generations. A FSIL can thus provide a bridge to positional cloning of quantitative trait loci (QTL) and marker-assisted selection in outcrossers ; and is particularly effective in exploiting the QTL mapping potential of crosses between selection lines or phenotypically differentiated populations that differ in frequency, but are not at fixation, for alternative QTL alleles. In the course of the power analyses, it is shown that for F2 and FSIL designs, power is a function of Nd# alone, where N is the total size of the mapping population and d is the standardized gene effect ; while for half-sib and full-sib populations, power is a function of Nd# and of the number of families included in the mapping population. This provides a convenient means of estimating power for a wide variety of mapping designs.

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