Peroxiredoxin 2 deficiency accelerates age-related ovarian failure through the reactive oxygen species-mediated JNK pathway in mice

Free Radical Biology & Medicine
Sun-Ji ParkDong-Seok Lee

Abstract

Reactive oxygen species (ROS) produced in biological reactions have been shown to contribute to ovarian aging. Peroxiredoxin 2 (Prx2) is an antioxidant enzyme that protects cells by scavenging ROS; however, its effect on age-related, oxidative stress-associated ovarian failure has not been reported. Here, we investigated its role in age-related ovarian dysfunction and 4-vinylcyclohexene diepoxide (VCD)-induced premature ovarian failure using Prx2-deficient mice. Compared to those in wildtype (WT) mice, serum levels of anti-Müllerian hormone, 17β-estradiol, and progesterone and numbers of follicles and corpora lutea were significantly lower in 18-month-old Prx2-/- mice. Moreover, levels of Bax, cytochrome c, cleaved caspase-3, and phosphorylated JNK proteins were higher and numbers of apoptotic (terminal deoxynucleotidyl transferase dUTP nick end labeling-positive) cells were considerably greater in 18-month-old Prx2-/- ovaries than WT ovaries. Furthermore, the effects of the ovarian toxicant VCD in significantly enhancing ROS levels and apoptosis through activation of JNK-mediated apoptotic signaling were more pronounced in Prx2-/- than WT mouse embryonic fibroblasts. Expression of the steroidogenic proteins StAR, CYP11A1, and ...Continue Reading

Citations

Mar 7, 2020·Archives of Physiology and Biochemistry·Jae-Ho KimSo-Young Park
Mar 12, 2020·Journal of Basic and Clinical Physiology and Pharmacology·Amos O AbolajiEbenezer O Farombi
May 10, 2020·BioMed Research International·Rui XuQinglin Zhang
Feb 1, 2020·Neurochemical Research·Jifei LiuZhenchang Zhang
Feb 27, 2020·Antioxidants·Young Jae Lee

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