The transcriptional factor Sox2 regulates the expression of some of the developmental genes, which are essential for the maintenance of pluripotency of stem cells. Sox2 also expresses in the female gamete during folliculogenesis, but its role remains ambiguous. The aim of this study was to investigate the expression of Sox2 in the mice ovarian tissue during different stage of estrous cycle. Adult National Medical Research Institute (NMRI) mice were considered as pro-estrous, estrous, met-estrous and di-estrous based on the cell type of the vaginal smear. Immunohistochemical staining of Sox2 marker was performed in mice ovarian tissue. Immunohistochemical staining revealed the expression of Sox2 in the cytoplasm of corpus luteum cells, stromal cells and oocyte. Our results suggest that adult mice ovaries accommodate cells carrying stem cell features. Manuscript profile

The goal of this study was to investigate the common clinical chemistry and distribution of xanthine oxidase (XO) in selected tissues of a mouse model of menopause. Twenty four NMRI female mice were divided into three groups: normal control (NC), and ovariectomized (OVX) groups and an estrogen-treated ovariectomized (OVX+E) group which received subcutaneous injection of estradiol benzoate (2 mg/kg). After 8 weeks, blood samples were collected for determining plasma clinical chemistry. Tissue XO activity was measured spectrophotometrically based on monitoring uric acid (UA) formation. Plasma levels of total cholesterol (TC), total protein (TP), albumin (ALB), globulin (G), and calcium, and enteric XO activity increased in OVX group as compared with NC group. Hepatic XO activity in OVX group declined in comparison with NC group. E2, TP, and G levels and liver and brain XO activities increased in OVX+E group when compared with OVX group. However, TC, high density lipoprotein cholesterol, UA, and ALB levels decreased in OVX+E group compared with OVX group. The brain and heart XO activities increased in OVX+E group as compared to that of NC group. XO activity was not detected in womb, spleen and stomach of all studied groups. XO activity was not detected in muscles of NC group while OVX and OVX+E groups showed muscle XO activity. Induction of ovariectomy produced a hypoestrogenic state that coincident with an adverse alteration of plasma clinical chemistry in mice. XO activity also changed after ovariectomy and estrogen-replacement therapy with a tissue-specific manner. Manuscript profile

Utilizing antioxidants offers a promising strategy for mitigating the effects of oxidative stress. This study was designed to assess the influence of alpha-lipoic acid (ALA) on the maturation of mouse oocytes and their apoptosis-related genes. Germinal vesicle oocytes, obtained from female mice aged 6-8 weeks, were subjected to in vitro maturation. Among these, 488 oocytes were exposed to 100 μM ALA, while 506 oocytes matured without ALA over a 16-hour duration. Subsequent evaluations were conducted to determine oocyte maturation rates. A portion of the mature oocytes at the metaphase II (MII) stage underwent in vitro fertilization, while the remaining oocytes were utilized to analyze the expression of Caspase 3, Bad, Bax, and Bcl2 through real-time RT-PCR. To quantify cell numbers, resulting blastocysts were stained with DAPI (4',6-diamidino-2-phenylindole). The group treated with ALA exhibited significantly higher rates of MII oocytes (77.30%) and a greater proportion of embryos developing into the blastocyst stage (33.87%) in comparison with the control group (55.81% and 25.06%, respectively; P<0.05). Moreover, the average cell count within blastocysts significantly increased in the ALA-treated group (82.37) compared to the control group (68.5; P<0.05). Furthermore, the pro-apoptotic genes expression decreased significantly, while the expression of the Bcl2 gene exhibited a significant increase in the ALA-treated group in comparison to the control group (P<0.05). In conclusion, the supplementation of the maturation medium for mouse oocytes with ALA resulted in improvements in oocyte development and overall embryo quality. This effect was attributed to the downregulation of pro-apoptotic genes and the upregulation of the anti-apoptotic gene. Manuscript profile