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Background : Environmental endocrine disruptor Di (2-ethylhexyl) phthalate (DEHP) widely affects the health of human and animals including the reproductive system. However, there are few studies on the protective strategies for the maternal DEHP exposure on follicular development of offspring. In the present study, we established a model of lactation female mice exposed to DEHP and reported the effects and potential mechanism of melatonin on the follicular development of offspring. Results: Our data showed that melatonin rescued the decrease of primordial follicles, antral follicles and oocyte number (increased by 74.2%) of offspring caused by maternal DEHP exposure from the primordial follicle formation stage. Proteomic analysis showed that melatonin altered the ovarian steroidogenesis, lipid metabolism, signal transduction, and DNA damage-related proteins. Melatonin reversed the disorder of lipid metabolism caused by DEHP and stabilized ovarian hormone secretase level. Molecular docking results indicated that DEHP/MEHP/melatonin binds to HSD17B2 to form a stable conformation, which may explain the reduction in 17β-estradiol induced by DEHP. Moreover, melatonin restored granulosa cell proliferation, reduced oxidative stress and DNA damage-related apoptosis, enhanced mitochondrial function, and protected ovarian cells. Besides, melatonin enhanced gap junction and promoted intercellular communication, which facilitate the formation of primordial follicles and the growth and development of antral follicles. In addition, melatonin rescued the oocyte defects of offspring caused by maternal DEHP exposure. Conclusions: Taken together, our data showed that melatonin could alleviate the damage of follicular development and abnormal ovarian steroidogenesis of offspring caused by maternal DEHP exposure. [ABSTRACT FROM AUTHOR]

ADP‐ribosylation factor 1 (Arf1) is a small GTPase belonging to the Arf family. As a molecular switch, Arf1 is found to regulate retrograde and intra‐Golgi transport, plasma membrane signaling, and organelle function during mitosis. This study aimed to explore the noncanonical roles of Arf1 in cell cycle regulation and cytoskeleton dynamics in meiosis with a mouse oocyte model. Arf1 accumulated in microtubules during oocyte meiosis, and the depletion of Arf1 led to the failure of polar body extrusion. Unlike mitosis, it finds that Arf1 affected Myt1 activity for cyclin B1/CDK1‐based G2/M transition, which disturbed oocyte meiotic resumption. Besides, Arf1 modulated GM130 for the dynamic changes in the Golgi apparatus and Rab35‐based vesicle transport during meiosis. Moreover, Arf1 is associated with Ran GTPase for TPX2 expression, further regulating the Aurora A–polo‐like kinase 1 pathway for meiotic spindle assembly and microtubule stability in oocytes. Further, exogenous Arf1 mRNA supplementation can significantly rescue these defects. In conclusion, results reported the noncanonical functions of Arf1 in G2/M transition and meiotic spindle organization in mouse oocytes. [ABSTRACT FROM AUTHOR]