17β-Estradiol alters oxidative stress response protein expression and oxidative damage in the uterus

Lisi Yuan, Alicia K. Dietrich, Ann M. Nardulli

Research output: Contribution to journalArticle

Abstract

The steroid hormone 17β-estradiol (E2) has profound effects on the uterus. However, with the E2-induced increase in uterine cell proliferation and metabolism comes increased production of reactive oxygen species (ROS). We examined the expression of an interactive network of oxidative stress response proteins including thioredoxin (Trx), Cu/Zn superoxide dismutase (SOD1), apurinic endonuclease (Ape1), and protein disulfide isomerase (PDI). We demonstrated that treatment of ovariectomized C57BL/6J female mice with E2 increased the mRNA and protein levels of Trx, but decreased SOD1 and Ape1 mRNA and protein expression. In contrast, E2 treatment increased PDI protein levels but had no effect on PDI transcript levels. Interestingly, E2 treatment also increased two markers of cellular damage, lipid peroxidation and protein carbonylation. Our studies suggest that the decreased expression of SOD1 and Ape1 caused by E2 treatment may in the long term result in disruption of ROS regulation and play a role in endometrial carcinogenesis.

Original languageEnglish (US)
Pages (from-to)218-226
Number of pages9
JournalMolecular and Cellular Endocrinology
Volume382
Issue number1
DOIs
StatePublished - Jan 25 2014

Keywords

  • Apurinic endonuclease
  • Cu/Zn superoxide dismutase
  • Estrogen receptor a{script}
  • Oxidative stress
  • Protein disulfide isomerase
  • Thioredoxin

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Endocrinology

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