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Summary Although the role of myo-inositol (MYO) in promoting the oocyte quality of PCOS patients has been documented in human studies; the cellular effects of this supplement on oocytes have not been directly examined due to ethical limitations. In the first phase of this study, MYO dosimetry was carried out simultaneously with the PCOS model development. An effective dose was obtained following the assessment of fasting insulin and testosterone levels using ELISA and ovarian morphology appraisal by histopathology. In the second phase, following the continuous administration of the effective dose of MYO and dehydroepiandrosterone (DHEA), cellular evaluation was performed. The quality of oocytes from superovulation was analyzed by examining maturity and normal morphology percentage using a stereomicroscope, intracellular reactive oxygen species (ROS) and glutathione (GSH) levels using fluorometry, and ATP count evaluation using ELISA. The results revealed that, among the four different MYO concentrations, the 0.36 mg/g dose compared with the DHEA group reduced testosterone levels and large atretic antral follicles (LAtAnF) diameter. This dose also increased the corpus luteum count and the granulosa:theca (G/T)layer thickness ratio in antral follicles. Furthermore, this dose increased mature oocytes and normal morphology percentage, ATP count, and GSH levels; however, it decreased ROS levels in mature oocytes. Our findings provide the grounds for further cellular and molecular studies on the PCOS mouse model, suggesting that the improvement in mitochondrial function and its antioxidant properties is probably one of the mechanisms by which MYO increases oocyte quality.

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Background: Hormonal imbalance is one of the important etiological factors for Oligoasthenoteratospermias (OAT). Objective: This study aimed to evaluate the effects of hormonal changes including prolactin, TSH, testosterone, luteinizing hormone, follicle-stimulating hormone, and anti-Mullerian hormone on sperm DNA fragmentation in normal men compared with OAT to design a clinical algorithm for the comprehensive study of male factor infertilities. Materials and Methods: We consecutively selected 60 candidates referred to the infertility clinic to collect the semen and blood samples. Then, a terminal deoxynucleotidyl transferase dUTP nick end labeling test was performed to evaluate the sperm DNA fragmentation index (DFI). After semen analysis and DFI checking, they were classified into 4 groups consisting of normospermia and OAT men each with or without increased DFI. Hormone parameters were analyzed using enzyme-linked immunoassay. Results: Follicle-stimulating hormone and luteinizing hormone levels showed positive correlations with DFI in a significant way (p ≤ 0.01), while testosterone and thyroidstimulating hormone were associated with sperm concentration. Prolactin and anti- Mullerian hormone levels significantly correlated (p ≤ 0.01) with sperm concentration and DFI value simultaneously. Conclusion: Decreased and increased levels of serum hormones could adversely affect semen profile and sperm DNA integrity which lead to severe male infertility. Although we investigated the effects of the main hormones related to male infertility on DNA damage, the role of these hormones on the fertilization rate and embryo quality needs to be evaluated in further studies. Key words: DNA fragmentation, Oligospermia, Asthenospermia, Teratospermia, Hormones.

Context: The SARS-CoV-2 virus causes dysfunction of vital organs in the body. Concerns about the destructive effect of SARS-CoV-2 on human reproductive tissues and fertility have increased. Evaluation of the possible mechanisms by which SARS-CoV-2 causes infertility is essential for effective prevention and treatment. This review aims to assess the studies that have been conducted on SARS-CoV-2 impacts on the human reproductive system. Evidence Acquisition: This review study investigated articles indexed in PubMed, Science-Direct, Scopus, and google scholar databases from 2019 to 2021. The Keywords SARS-CoV-2, COVID-19, human reproductive system, testis, and ovary were searched in the mentioned databases. Results: The present study assessed the expression of SARS-CoV-2-specific receptors, the presence of the virus in the human reproductive system, and the mechanisms by which this virus can affect human fertility. Conclusions: SARS-CoV-2, like other viruses, may indirectly influence the male reproductive system through cytokine storms, inflammation-causing oxidative stress, and its possible complications. The direct effects of SARS-CoV-2 on the male reproductive system are also reported. The testis may be a potential target for the SARS-CoV-2 virus. The impact of the SARS-CoV-2 virus on women's reproductive performance is unknown and requires further investigation.