Dietary Selenium Supplementation Ameliorates Female Reproductive Efficiency in Aging Mice

Abstract

Female reproductive (ovarian) aging is distinctively characterized by a markedly reduced reproductive function due to a remarkable decline in quality and quantity of follicles and oocytes. Selenium (Se) has been implicated in playing many important biological roles in male fertility and reproduction; however, its potential roles in female reproduction, particularly in aging subjects, remain poorly elucidated. Therefore, in the current study we used a murine model of female reproductive aging and elucidated how different Se-levels might affect the reproductive efficiency in aging females. Our results showed that at the end of an 8-week dietary trial, whole-blood Se concentration and blood total antioxidant capacity (TAOC) were significantly reduced in Se-deficient (0.08 mg Se/kg; Se-D) mice, whereas both of these biomarkers were significantly higher in inorganic (0.33 mg/kg; ISe-S) and organic (0.33 mg/kg; OSe-S) Se-supplemented groups. Similarly, compared to the Se-D group, Se supplementation significantly ameliorated the maintenance of follicles and reduced the rate of apoptosis in ovaries. Meanwhile, the rate of in vitro-produced embryos resulting from germinal vesicle (GV) oocytes was also significantly improved in Se-supplemented (ISe-S and OSe-S) groups compared to the Se-D mice, in which none of the embryos developed to the hatched blastocyst stage. RT-qPCR results revealed that mRNA expression of Gpx1, Gpx3, Gpx4, Selenof, p21, and Bcl-2 genes in ovaries of aging mice was differentially modulated by dietary Se levels. A considerably higher mRNA expression of Gpx1, Gpx3, Gpx4, and Selenof was observed in Se-supplemented groups compared to the Se-D group. Similarly, mRNA expression of Bcl-2 and p21 was significantly lower in Se-supplemented groups. Immunohistochemical assay also revealed a significantly higher expression of GPX4 in Se-supplemented mice. Our results reasonably indicate that Se deficiency (or marginal levels) can negatively impact the fertility and reproduction in females, particularly those of an advancing age, and that the Se supplementation (inorganic and organic) can substantiate ovarian function and overall reproductive efficiency in aging females.

Characterization of Glutathione Peroxidase 4 in Rat Oocytes, Preimplantation Embryos, and Selected Maternal Tissues during Early Development and Implantation

“…GPx4 is localized in several organs that have a direct or indirect relation to reproduction, such as reproductive organs (testis and oviduct), thyroid gland, and hypophysis [ 37 ]. Our result that GPx4 is present in rat ovary supports the finding of Yang et al (2019) who reported the same finding [ 38 ]. GPx4 in this organ could play a role in the development of follicles because GPx4 can decrease levels of ROS and subsequently OS [ 39 ].…”

Disturbances in Thyroid Hormone Metabolism in Rats Exposed to γ- Radiation and Carbon Tetrachloride: The Role of N- acetyl cysteine and Sodium Selenite

“…Group 1 (control) animals of this group were kept as control. Group 2 (NAC +Se) animals were orally supplemented with NAC dissolved in distilled water at a dose level of 200 mg/kg (according to Maheswari et al, 2014) and Se dissolved in distilled water at a dose level of 0.4 mg/kg (based on Said et al, 2012;Yang et al 2019), daily for two weeks. Group 3 (Rad) rats were whole-body exposed to gamma radiation at a dose level of 6 Gy.…”

The Protective Effect of Aspirin Eugenol Ester on Oxidative Stress to PC12 Cells Stimulated with H2O2 through Regulating PI3K/Akt Signal Pathway

“…Previous studies found that H 2 O 2 could cause excessive accumulation of intracellular ROS, mtROS, and superoxide anion in PC12 cells. AEE pretreatment could reduce the increase of [71]. Studies showed that H 2 O 2 induced PC12 cells could produce excessive MDA, intracellular ROS, and mtROS and significantly reduce the activities of SOD, GSH-Px, and CAT.…”

“…SOD catalyzes the conversion of superoxide radicals to O 2 and H 2 O 2 , while CAT catalyzes dismutation reactions of H 2 O 2 into H 2 O [ 69 , 70 ]. GSH-PX prevents the formation of toxic hydroxyl and peroxyl radicals via providing electrons to H 2 O 2 and lipid peroxides [ 71 ]. Studies showed that H 2 O 2 induced PC12 cells could produce excessive MDA, intracellular ROS, and mtROS and significantly reduce the activities of SOD, GSH-Px, and CAT.…”