Resveratrol enhanced mitochondrial recovery from cryopreservation‐induced damages in oocytes and embryos

Abstract Background Mitochondria play a crucial role in nuclear maturation, fertilization, and subsequent embryo development. Cryopreservation is an important assisted reproductive technology that is used worldwide for humans and domestic animals. Although mitochondrial quantity and quality are deci...

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Bibliographic Details
Main Author: Hisataka Iwata
Format: Article
Language:English
Published: Wiley 2021-10-01
Series:Reproductive Medicine and Biology
Subjects:
Online Access:https://doi.org/10.1002/rmb2.12401
Description
Summary:Abstract Background Mitochondria play a crucial role in nuclear maturation, fertilization, and subsequent embryo development. Cryopreservation is an important assisted reproductive technology that is used worldwide for humans and domestic animals. Although mitochondrial quantity and quality are decisive factors for successful development of oocytes and embryos, cryopreservation induces mitochondrial dysfunction. Upon thawing, the damaged mitochondria are removed, and de novo synthesis occurs to restore the function of mitochondria. Resveratrol, 3,5,4′‐trihydroxystilbene, is a polyphenolic antioxidant that has versatile target proteins, among which sirtuin‐1 (SIRT1) is a key regulator of in mitochondrial biogenesis and degradation. Methods The present study is a literature review focusing on experiments involving the hypothesis that the activation of mitochondrial biogenesis and degradation following cryopreservation and warming by resveratrol may help mitochondrial recovery and improve oocyte and embryo development. Main findings and conclusion Resveratrol improves oocyte maturation and development and upregulates mitochondrial biogenesis and degradation. When vitrified‐warmed embryos are treated with resveratrol, it helps in mitochondrial regulation and recovery of embryos from cryopreservation‐induced damage. Conclusion Resveratrol treatment is a possible countermeasure against cryopreservation‐induced mitochondrial damage.
ISSN:1445-5781
1447-0578