PMID- 33612552
OWN - NLM
STAT- MEDLINE
DCOM- 20211220
LR  - 20211220
IS  - 1348-4400 (Electronic)
IS  - 0916-8818 (Print)
IS  - 0916-8818 (Linking)
VI  - 67
IP  - 2
DP  - 2021 Apr 21
TI  - Mitochondrial reactive oxygen species regulate mitochondrial biogenesis in 
      porcine embryos.
PG  - 141-147
LID - 10.1262/jrd.2020-111 [doi]
AB  - The number of mitochondria in blastocysts is a potential marker of embryo 
      quality. However, the molecular mechanisms governing the mitochondrial number in 
      embryos are unclear. This study was conducted to investigate the effect of 
      reduced mitochondrial reactive oxygen species (ROS) levels on mitochondrial 
      biogenesis in porcine embryos. Oocytes were collected from gilt ovaries and 
      activated to generate over 4 cell-stage embryos at day 2 after activation. These 
      embryos were cultured in media containing either 0.1 muM MitoTEMPOL (MitoT), 0.5 
      muM Mitoquinol (MitoQ), or vehicle (ethanol) for 5 days to determine the rate of 
      development to the blastocyst stage. The mitochondrial number in blastocysts was 
      evaluated by real-time polymerase chain reaction (PCR). Five days after 
      activation, the embryos (early morula stage) were subjected to immunostaining to 
      determine the expression levels of NRF2 in the nucleus. In addition, the 
      expression levels of PGC1alpha and TFAM in the embryos were examined by reverse 
      transcription PCR. One day of incubation with the antioxidants reduced the ROS 
      content in the embryos but did not affect the rate of development to the 
      blastocyst stage. Blastocysts developed in medium containing MitoT had lower 
      mitochondrial DNA copy numbers and ATP content, whereas MitoQ showed similar but 
      insignificantly trends. Treatment of embryos with either MitoT or MitoQ decreased 
      the expression levels of NRF2 in the nucleus and levels of PGC1alpha and TFAM. These 
      findings indicate that reductions in mitochondrial ROS levels are associated with 
      low mitochondrial biogenesis in embryos.
FAU - Kageyama, Mio
AU  - Kageyama M
AD  - Department of Animal Science, Tokyo University of Agriculture, Kanagawa 243-0034, 
      Japan.
FAU - Ito, Jun
AU  - Ito J
AD  - Department of Animal Science, Tokyo University of Agriculture, Kanagawa 243-0034, 
      Japan.
FAU - Shirasuna, Koumei
AU  - Shirasuna K
AD  - Department of Animal Science, Tokyo University of Agriculture, Kanagawa 243-0034, 
      Japan.
FAU - Kuwayama, Takehito
AU  - Kuwayama T
AD  - Department of Animal Science, Tokyo University of Agriculture, Kanagawa 243-0034, 
      Japan.
FAU - Iwata, Hisataka
AU  - Iwata H
AD  - Department of Animal Science, Tokyo University of Agriculture, Kanagawa 243-0034, 
      Japan.
LA  - eng
PT  - Journal Article
DEP - 20210220
PL  - Japan
TA  - J Reprod Dev
JT  - The Journal of reproduction and development
JID - 9438792
RN  - 0 (Antioxidants)
RN  - 0 (DNA, Mitochondrial)
RN  - 0 (NF-E2-Related Factor 2)
RN  - 0 (Reactive Oxygen Species)
SB  - IM
MH  - Animals
MH  - Antioxidants/metabolism/pharmacology
MH  - Blastocyst
MH  - DNA, Mitochondrial/metabolism
MH  - Embryo, Mammalian/*metabolism
MH  - Embryonic Development/drug effects
MH  - Female
MH  - Gene Dosage
MH  - Insemination, Artificial/*veterinary
MH  - Mitochondria/*metabolism
MH  - Morula/metabolism
MH  - NF-E2-Related Factor 2/metabolism
MH  - Oocytes/cytology
MH  - Organelle Biogenesis
MH  - Parthenogenesis
MH  - Polymerase Chain Reaction
MH  - *Reactive Oxygen Species
MH  - Swine
PMC - PMC8075724
OTO - NOTNLM
OT  - Blastocyst
OT  - Embryo development
OT  - Mitochondrial biogenesis
OT  - Mitochondrial number
OT  - Reactive oxygen species
COIS- The authors declare that there are no conflicts of interest regarding this study.
EDAT- 2021/02/23 06:00
MHDA- 2021/12/21 06:00
PMCR- 2021/04/01
CRDT- 2021/02/22 05:50
PHST- 2021/02/23 06:00 [pubmed]
PHST- 2021/12/21 06:00 [medline]
PHST- 2021/02/22 05:50 [entrez]
PHST- 2021/04/01 00:00 [pmc-release]
AID - 2020-111 [pii]
AID - 10.1262/jrd.2020-111 [doi]
PST - ppublish
SO  - J Reprod Dev. 2021 Apr 21;67(2):141-147. doi: 10.1262/jrd.2020-111. Epub 2021 Feb 
      20.