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This study, using an in vitro ovary culture model, investigates the mechanisms through which Di (2-ethylhexyl) phthalate (DEHP) impairs germ cell cyst breakdown and primordial follicle assembly. The results indicate the latter effects exerted by 10 or 100 μM DEHP in cultured newborn ovaries were associated with increased levels of reactive oxygen species (ROS) and apoptosis. Based on a transcriptome analysis, we detected the expression of the oxidative stress-related gene Xdh (xanthine dehydrogenase) was significantly up-regulated in DEHP cultured ovaries. Two treatments, namely Xdh RNAi or the addition of melatonin to the ovary culture, inhibited the increase of Xdh expression and ROS levels caused by DEHP and, at the same time, reduced apoptosis and the impairment of primordial follicle assembly in the treated ovaries. Together, the results identify Xdh gene as one of the major targets of DEHP in newborn ovaries and that the consequent increased level of ROS is possibly responsible for the increment of apoptosis and primordial follicle assembly impairment. At the same time, they highlight that melatonin alleviates the effects of DEHP as with other endocrine disrupting compounds on the ovary. This article is protected by copyright. All rights reserved.
This article was published in the following journal.
Name: Journal of pineal research
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