Mitochondrial reactive oxygen species regulate mitochondrial biogenesis in porcine embryos

Abstract

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 µM MitoTEMPOL (MitoT), 0.5 µM 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 PGC1α 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 PGC1α and TFAM. These findings indicate that reductions in mitochondrial ROS levels are associated with low mitochondrial biogenesis in embryos.

Double-edged sword: effects of human sperm reactive oxygen species on embryo development in IVF cycles

“…The suitable concentration of mitochondrial ROS is an important signaling messenger and has been shown to promote the proliferation and differentiation of the embryo. Reducing the mitochondrial ROS level of the pig embryo will weaken embryo mitochondrial biogenesis [ 32 ]. We hypothesized that mROS carried by sperm are distributed among the blastomeres along with sperm mitochondria after fusing with oocytes, which may just fill the gap of oocyte mROS.…”

Double-edged sword: Effects of human sperm reactive oxygen species on embryo development in IVF cycles

“…The suitable concentration of mitochondrial ROS is an important signaling messenger and has been shown to promote the proliferation and differentiation of the embryo. Reducing the mitochondrial ROS level of the pig embryo will weaken embryo mitochondrial biogenesis [32]. We hypothesized that mROS carried by sperm are distributed among the blastomeres along with sperm mitochondria after fusing with oocytes, which may just ll the gap of oocyte mROS.…”

Revolutionizing bone regeneration: advanced biomaterials for healing compromised bone defects

“…These defenses are mechanistic antioxidant enzymes expressed and secreted by tissues to reduce the accumulation of ROS or free radicals involved in the aging process. Mitochondrial ROS are highly reactive molecules produced as natural byproducts of cellular respiration within the mitochondria (Kageyama et al, 2021). While mitochondria are essential for generating energy in the form of ATP, they can also generate ROS during this process.…”

“…In low levels, ROS can regulate cellular functions such as cell proliferation, apoptosis, and immune response. However, excessive accumulation of mitochondrial ROS can lead to oxidative damage of cellular components, including DNA, proteins, and lipids, contributing to the development of various diseases and aging processes (Hernansanz-Agustín and Enríquez, 2021;Kageyama et al, 2021). Therefore, maintaining a delicate balance of mitochondrial ROS is crucial for cellular health and overall wellbeing.…”