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Selenium supplementation induces mitochondrial biogenesis in trophoblasts
A. Khera, LF. Dong, O. Holland, J. Vanderlelie, EA. Pasdar, J. Neuzil, AV. Perkins,
Jazyk angličtina Země Anglie, Velká Británie
Typ dokumentu časopisecké články, práce podpořená grantem
- MeSH
- biogeneze organel * MeSH
- buněčné linie MeSH
- DNA vazebné proteiny metabolismus MeSH
- faktor 1 související s NF-E2 metabolismus MeSH
- lidé MeSH
- mitochondrie účinky léků metabolismus MeSH
- placenta účinky léků metabolismus MeSH
- reaktivní formy kyslíku metabolismus MeSH
- selen aplikace a dávkování MeSH
- selenoproteiny metabolismus MeSH
- těhotenství MeSH
- transkripční faktory metabolismus MeSH
- trofoblasty účinky léků metabolismus MeSH
- upregulace účinky léků MeSH
- Check Tag
- lidé MeSH
- těhotenství MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
INTRODUCTION: Placental oxidative stress has been implicated in pregnancy complications and previous work has shown that selenium can protect trophoblast mitochondria from oxidative stress. This report examines mitochondrial function and content in trophoblasts supplemented with selenium. METHODS: Swan-71, JEG-3 and BeWo cells and placental tissue were incubated with sodium selenite or selenomethionine. Mitochondrial function was examined in a respirometer. Mitochondrial content was determined using RT-PCR. The levels of the mitochondrial biogenesis markers selenoprotein H, PGC-1α and NRF-1 was examined by western blotting. RESULTS: Mitochondrial respiration was significantly enhanced post selenium supplementation in cells and tissues. Selenium supplementation increased mitochondrial content and up-regulated mitochondrial biogenesis mediators in cells. DISCUSSION: These results emphasise the importance of selenium in mitochondrial regeneration in trophoblasts.
Citace poskytuje Crossref.org
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- $a INTRODUCTION: Placental oxidative stress has been implicated in pregnancy complications and previous work has shown that selenium can protect trophoblast mitochondria from oxidative stress. This report examines mitochondrial function and content in trophoblasts supplemented with selenium. METHODS: Swan-71, JEG-3 and BeWo cells and placental tissue were incubated with sodium selenite or selenomethionine. Mitochondrial function was examined in a respirometer. Mitochondrial content was determined using RT-PCR. The levels of the mitochondrial biogenesis markers selenoprotein H, PGC-1α and NRF-1 was examined by western blotting. RESULTS: Mitochondrial respiration was significantly enhanced post selenium supplementation in cells and tissues. Selenium supplementation increased mitochondrial content and up-regulated mitochondrial biogenesis mediators in cells. DISCUSSION: These results emphasise the importance of selenium in mitochondrial regeneration in trophoblasts.
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