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青春期小鼠睾丸碳离子辐射诱导急性损伤的比较蛋白质组学分析及可能的毒理学机制

Comparative proteomic profiling and possible toxicological mechanism of acute injury induced by carbon ion radiation in pubertal mice testes.

作者信息

Li Hongyan, Zhang Hong, Di Cuixia, Xie Yi, Zhou Xin, Yan Jiawei, Zhao Qiuyue

机构信息

Department of Heavy Ion Radiation Medicine, Institute of Modern Physics, Chinese Academy of Sciences, Lanzhou 730000, China; Key Laboratory of Heavy Ion Radiation Biology and Medicine of Chinese Academy of Sciences, Lanzhou 730000, China; Key Laboratory of Heavy Ion Radiation Medicine of Gansu Province, Lanzhou 730000, China.

Department of Heavy Ion Radiation Medicine, Institute of Modern Physics, Chinese Academy of Sciences, Lanzhou 730000, China; Key Laboratory of Heavy Ion Radiation Biology and Medicine of Chinese Academy of Sciences, Lanzhou 730000, China; Key Laboratory of Heavy Ion Radiation Medicine of Gansu Province, Lanzhou 730000, China.

出版信息

Reprod Toxicol. 2015 Dec;58:45-53. doi: 10.1016/j.reprotox.2015.07.079. Epub 2015 Aug 6.

Abstract

We investigated potential mechanisms of acute injury in pubertal mice testes after exposure to carbon ion radiation (CIR). Serum testosterone was measured following whole-body irradiation with a 2Gy carbon ion beam. Comparative proteomic profiling and Western blotting were applied to identify potential biomarkers and measure protein expression, and terminal dUTP nick end-labeling (TUNEL) was performed to detect apoptotic cells. Immunohistochemistry and immunofluorescence were used to investigate protein localization. Serum testosterone was lowest at 24h after CIR, and 10 differentially expressed proteins were identified at this time point that included eIF4E, an important regulator of initiation that combines with mTOR and 4EBP1 to control protein synthesis via the mTOR signaling pathway during proliferation and apoptosis. Protein expression and localization studies confirmed their association with acute injury following exposure to CIR. These three proteins may be useful molecular markers for detecting abnormal spermatogenesis following exposure to environmental and therapeutic radiation.

摘要

我们研究了青春期小鼠睾丸在暴露于碳离子辐射(CIR)后急性损伤的潜在机制。用2Gy碳离子束进行全身照射后测量血清睾酮。应用比较蛋白质组学分析和蛋白质印迹法来鉴定潜在的生物标志物并测量蛋白质表达,并进行末端脱氧核苷酸转移酶介导的缺口末端标记法(TUNEL)以检测凋亡细胞。免疫组织化学和免疫荧光用于研究蛋白质定位。血清睾酮在CIR后24小时最低,此时鉴定出10种差异表达的蛋白质,其中包括eIF4E,它是起始的重要调节因子,在增殖和凋亡过程中通过mTOR信号通路与mTOR和4EBP1结合以控制蛋白质合成。蛋白质表达和定位研究证实了它们与暴露于CIR后的急性损伤有关。这三种蛋白质可能是检测暴露于环境辐射和治疗性辐射后异常精子发生的有用分子标志物。

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