17β-Estradiol alters oxidative damage and oxidative stress response protein expression in the mouse mammary gland

被引:6
|
作者
Yuan, Lisi [1 ]
Dietrich, Alicia K. [1 ]
Ziegler, Yvonne S. [1 ]
Nardulli, Ann M. [1 ]
机构
[1] Univ Illinois, Dept Mol & Integrat Physiol, 524 Burrill Hall,407 South Goodwin Ave, Urbana, IL 61801 USA
关键词
17; beta-estradiol; Estrogen receptor alpha; Superoxide dismutase; Apurinic endonuclease; Oxidative stress; Mammary gland; ESTROGEN-RECEPTOR-ALPHA; DNA-REPAIR; PROGESTERONE RECEPTORS; PERSISTENT CHANGES; CANCER STATISTICS; TUMORIGENESIS; TRANSCRIPTION; GENE; ESTRADIOL; PREGNANCY;
D O I
10.1016/j.mce.2016.02.007
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Although substantial evidence has demonstrated that parity and 17 beta-estradiol (E2) reduce mammary carcinogenesis, it is not clear how this protection is conferred. Thus, we examined the effects of parity and E2 treatment in the mammary glands of ovariectomized 15 week-old virgin mice, 15 week-old primiparous mice, and 9 month-old retired breeders. E2 treatment significantly increased lipid peroxidation, protein carbonylation, and protein nitrosylation in the virgin mice, but not in the age-matched primiparous mice or retired breeders. Mammary gland expression of the oxidative stress response protein Cu/Zn superoxide dismutase was consistently reduced in all of the E2-treated mice regardless of parity. Expression of the oxidative stress and DNA repair protein apurinic endonuclease (Ape1) was significantly increased only in the mammary glands of the E2-treated retired breeders. These findings suggest that E2 and parity help to reduce mammary oncogenesis by maintaining the structure and function of proteins, lipids, and DNA. (C) 2016 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:11 / 21
页数:11
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