Mitochondria are the major site of reactive oxygen species (ROS) and excessive ROS causes cellular damage and has been associated with complication of pregnancy such as preeclampsia. In previous studies(1) we have Selenium has been shown to protect and scavenge the trophoblast cells through the antioxidant enzymes Gpx and Thx-Red, when they induce free radicals (Khera et al; 2013). The present study is conducted to demonstrate how selenium increases mitochondrial function of the trophoblast cells and activates mitochondrial biogenesis through various pathways which further activates transcription factors such as nuclear respiratory factor-1 (NRF1) and peroxisome proliferator-activated receptor coactivator -1alpha (PGC-1α) (Mehta et al;2012).
Trophoblast cells (BeWo, JEG-3 and Swan-71) were treated with Na Selenite (100nM) for 24 hours. Cellular respiration was then measured from an Oxygraph-2k Oroboros high respirometry chamber operated at 37°C. The qPCR experiment and citrate synthase experiment were done to demonstrate that selenium treated cells have higher mitochondrial number.
The study conducted on trophoblast cells exposed to selenium supplementation revealed that selenium treatment (100 nM) for 24 hours effectively increases the mitochondrial number and biogenesis. The oxygen consumption was higher in the cells treated with NaSe as compared to the non-treated cells. The mitochondrial respiration indicated that oxygen flow was significantly increased in selenium supplemented cells. qPCR data revealed that mitochondrial ratio was also higher in the cells treated with selenium.
These data suggest that selenium increases mitochondrial biogenesis. The benefit side of selenium is mediated through lowering ROS production and thus protecting mitochondrial function. This gives the special importance of maintaining adequate selenium during pregnancy and especially in pregnancies complicated by conditions such as preeclampsia.