Glutathione Ethyl Ester Protects In Vitro-Maturing Bovine Oocytes against Oxidative Stress Induced by Subsequent Vitrification/Warming.
Tania García-MartínezMeritxell Vendrell-FlotatsIris Martínez-RoderoErika Alina Ordóñez-LeónManuel Álvarez-RodriguezManel López-BejarMichael L DustinTeresa MogasPublished in: International journal of molecular sciences (2020)
This study aimed to examine whether the addition of glutathione ethyl ester (GSH-OEt) to the in vitro maturation (IVM) medium would improve the resilience of bovine oocytes to withstand vitrification. The effects of GSH-OEt on spindle morphology, levels of reactive oxygen species (ROS), mitochondrial activity and distribution, and embryo developmental potential were assessed together with the expression of genes with a role in apoptosis (BAX, BCL2), oxidative-stress pathways (GPX1, SOD1), water channels (AQP3), implantation (IFN-τ) and gap junctions (CX43) in oocytes and their derived blastocysts. Vitrification gave rise to abnormal spindle microtubule configurations and elevated ROS levels. Supplementation of IVM medium with GSH-OEt before vitrification preserved mitochondrial distribution pattern and diminished both cytoplasmic and mitochondrial ROS contents and percentages of embryos developing beyond the 8-cell stage were similar to those recorded in fresh non-vitrified oocytes. Although not significantly different from control vitrified oocytes, vitrified oocytes after GSH-OEt treatment gave rise to similar day 8-blastocyst and hatching rates to fresh non-vitrified oocytes. No effects of GSH-OEt supplementation were noted on the targeted gene expression of oocytes and derived blastocysts, with the exception of GPX1, AQP3 and CX43 in derived blastocysts. The addition of GSH-OEt to the IVM medium before vitrification may be beneficial for embryo development presumably as the consequence of additional anti-oxidant protection during IVM.
Keyphrases
- oxidative stress
- reactive oxygen species
- dna damage
- fluorescent probe
- gene expression
- cell death
- induced apoptosis
- diabetic rats
- ischemia reperfusion injury
- immune response
- climate change
- dna methylation
- mesenchymal stem cells
- poor prognosis
- depressive symptoms
- social support
- ionic liquid
- binding protein
- single cell
- cell cycle arrest
- signaling pathway
- pi k akt