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 cryo-preservation 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 em-bryos derived from vitrified-warmed oocytes through SIRT1. The results showed that the reactive oxygen species levels increased, the glutathione levels and SIRT1 expression decreased significantly in parthe-nogenetic 2-cell embryos derived from cryopreserved oocyte, and the parthenogenetic blastocyst for-mation rates significantly decreased when compared to those derived from control oocytes. These unfavorable phenomena were prevented by the addition of either 10-9 mol/L melatonin or 10-6 mol/L SRT-1720 (SIRT1 agonist), and it was restored by the supplementation of 10-9 mol/L melatonin in combination with 2 x 10-5 mol/L EX527 (SIRT1 inhibitor). Therefore, the findings from the present study concluded that melatonin may reduce oxidative stress via regulating SIRT1, and potentially promote the parthenogenetic development of vitrified-warmed mouse MII oocytes.& COPY; 2023 Elsevier Inc. All rights reserved.

Automated summary

This study investigates whether melatonin can modulate oxidative stress in parthenogenetic 2-cell embryos derived from vitrified-warmed oocytes through SIRT1. The results demonstrate that melatonin can reduce oxidative stress by regulating SIRT1 and promote the development of vitrified-warmed mouse MII oocytes.