The walnut-derived peptide TW-7 improves mouse parthenogenetic embryo development of vitrified MII oocytes potentially by promoting histone lactylation.

Background: Previous studies have shown that the vitrification of metaphase II (MII) oocytes significantly represses their developmental potential. Abnormally increased oxidative stress is the probable factor; however, the underlying mechanism remains unclear. The walnut-derived peptide TW-7 was initially isolated and purified from walnut protein hydrolysate.

Melatonin promotes parthenogenetic development of vitrified-warmed mouse MII oocytes, potentially by reducing oxidative stress through SIRT1.

Previous studies have demonstrated that melatonin could ameliorate oxidative stress during the cryopreservation of mouse MII oocytes and their in vitro culture after parthenogenetic activation. However, the underlying molecular mechanism remained poorly understood. This study was conducted to investigate whether melatonin could modulate the oxidative stress in the parthenogenetic 2-cell embryos derived from vitrified-warmed oocytes through SIRT1.

Chiral MoSe Nanoparticles for Ultrasensitive Monitoring of Reactive Oxygen Species In Vivo.

Reactive oxygen species (ROS) are involved in neurodegenerative diseases, cancer, and acute hepatitis, and quantification of ROS is critical for the early diagnosis of these diseases. In this work, a novel probe is developed, based on chiral molybdenum diselenide (MoSe ) nanoparticles (NPs) modified by the fluorescent molecule, cyanine 3 (Cy3). Chiral MoSe NPs show intensive circular dichroism (CD) signals at 390 and 550 nm, whereas the fluorescence of Cy3 at 560 nm is quenched by MoSe NPs.

Oxidative Stress and Oocyte Cryopreservation: Recent Advances in Mitigation Strategies Involving Antioxidants.

Oocyte cryopreservation is widely used in assisted-reproductive technology and animal production. However, cryopreservation not only induces a massive accumulation of reactive oxygen species (ROS) in oocytes, but also leads to oxidative-stress-inflicted damage to mitochondria and the endoplasmic reticulum. These stresses lead to damage to the spindle, DNA, proteins, and lipids, ultimately reducing the developmental potential of oocytes both in vitro and in vivo.