Data for: Relevance of di-(2-ethylhexyl) phthalate induced prepuberal testicular injury to increased m6A RNA modification via inhibition of Nrf2-mediated antioxidant response

Published: 9 January 2020| Version 1 | DOI: 10.17632/8sbkzysnz6.1
Tianxin Zhao, shengde wu, chengjun yu, Yihang Yu, Jiandong Lu, Jie Zhao, Dawei He, Tao Lin, Chunlan Long, Yi Wei, Mang Sun, Bin Liu, Junke Wang, Lindong Han, Lianju Shen, Zhou Yu, Guanghui Wei, Zhaoying Wang, Huan Wu, qinlin shi, Yuexin Wei


Exposure to DEHP at the prepuberty stage could lead to prepuberal testicular injury, but the specific mechanism is unclear. This study used a gavage method to expose Sprague-Dawley (SD) rats with DEHP at prepuberty stage to 0, 250, and 500 mg/kg of body weight per day from postnatal day 22 (PND21) to PND 35. The testicular injury and oxidative stress were evaluated, and the level of 6-methyladenosine (m6A) modification and expression of modulator genes for RNA methylation were detected in testes. Furthermore, the m6A modification of important antioxidant transcription factor Nrf2 was analyzed using methylated RNA immunoprecipitation qPCR. Our results showed that DEHP destroyed testicular histological morphology, decreased testosterone concentrations, down-regulated expression of spermatogenesis inducers, enhanced oxidative stress, inhibited the Nrf2-mediated antioxidant pathway, and increased apoptosis in testes. Additionally, DEHP improved global levels of m6A modification in total RNA and altered the expression of two important RNA methylation modulator genes, FTO and YTHDC2. Moreover, the m6A modification of Nrf2 mRNA increased with DEHP exposure.



Antioxidant Capacity, RNA Methylation, Phthalate, Antioxidant Study