The reduction of female fertility over time is considered as a natural consequence of ovarian aging. The exact mechanism underlying this process is not fully elucidated. However, it is becoming increasingly evident that qualitative and quantitative mitochondrial genome alterations might play a relevant role. The former include mitochondrial DNA (mtDNA) damage caused by oxidative stress, the accumulation of acquired mtDNA mutations, the effects of inherited mtDNA mutations, and alterations in the mitochondrial stress response mechanism. The latter refer to alterations in the oocytes, granuolosa cells, and embryonic cells mtDNA content. The present review aims to investigate the evidence about: (1) the effect of qualitative and quantitative mtDNA alterations on female fertility, paying particular attention to those with a pathophysiology characterized by a relevant role of oxidative stress; (2) the use of oocytes, granulosa cells (GCs), embryonic cells, and peripheral blood cells mtDNA copy number as a female fertility surrogate biomarker; (3) experimental therapies tested to try to subvert the ovarian aging process with particular reference to antioxidant treatments.

Purpose Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the virus behind the COVID-19 pandemic, affects multiple organs, including the male reproductive system. While viral infections can harm male fertility through cytokine storms, the effects of SARS-CoV-2 on fertility are still unclear. Thus, this study aimed to examine the persistence of viral RNA and inflammatory responses in semen following SARS-CoV-2 infection and the safety of conventional freezing and vitrification techniques. Methods Semen samples from 20 patients were collected 3 months post-SARS-CoV-2 infection. Samples underwent freezing and vitrification. Molecular and cellular analysis separated seminal plasma and pellets. Flow cytometry characterized immune cells. Viral RNA was extracted from plasma and sperm, followed by RT-qPCR. Cytometric Bead Array measured cytokine levels. Results Angiotensin-converting enzyme 2 (ACE2) and transmembrane serine protease 2 (TMPRSS2) receptors were detected in both plasma and sperm fractions. Five patients exhibited viral RNA-dependent RNA polymerase, indicating potential persistence. Elevated inflammatory cytokines in plasma implied persistent inflammation affecting sperm vitality. Immune cells associated with viral clearance were identified in semen, correlating with receptor expression and cytokines. Both conventional freezing and vitrification were found safe procedures for preserving male fertility. Conclusions Our study highlights the impact of SARS-CoV-2 on male reproductive health, emphasizing the persistence of viral entry receptors, potential viral RNA presence, the inflammatory environment, and the involvement of immune populations in the male reproductive tract post-infection. Importantly, we confirm the safety of conventional freezing and vitrification techniques for preserving male fertility in assisted reproductive technology programs amidst the COVID-19 pandemic.