Effects of Coenzyme Q10 Supplemented to Culture Medium on Morphology of Mouse Early Embryonic Development as a Model for Human Being

2020 ◽  
Vol 24 (4) ◽  
pp. 7267-7272
Author(s):  
Dr. Muhammad Baqir MR Fakhrildin
2019 ◽  
Vol 119 (2) ◽  
pp. 2
Author(s):  
Caitlin Streacker ◽  
Brian D. Whitaker

The objective of this study was to determine the reduction of polyspermic penetration, and increase of mitochondrial activity, in early pig embryonic development by supplementing different concentrations of coenzyme Q10 during oocyte maturation. Oocytes (n = 1,100) were supplemented during the last 24 h of maturation with 0 (control), 10, 50, or 100 μM of coenzyme Q10. After in vitro fertilization (IVF), embryos were evaluated for fertilization kinetics (penetration, polyspermic penetration, male pronuclear formation), and subsequent embryonic development and mitochondrial activity. Supplementation of 100 μM coenzyme Q10 was detrimental to the oocytes, as they had significantly lower (p < 0.05) fertilization kinetic and early embryonic development rates to the other treatment groups. There were no differences in fertilization kinetic and early embryonic development rates between the 0, 10 and 50 μM coenzyme Q10 treatment groups. Oocytes, matured in medium supplemented with 50 μM coenzyme Q10, ultimately developed into embryos with a significantly greater (p < 0.05) presence of intact mitochondrial membranes (observed at both 48 and 144 h post-IVF) compared to oocytes not supplemented with coenzyme Q10. In summary, supplementation of 100 μM coenzyme Q10 during oocyte maturation is detrimental, yet supplementation of 50 μM coenzyme Q10 leads to a higher occurrence of intact mitochondrial membranes in the in vitro produced pig embryos.


2004 ◽  
Vol 16 (2) ◽  
pp. 191 ◽  
Author(s):  
F.N. Scenna ◽  
J.L. Edwards ◽  
F.N. Schrick

Several studies have implicated prostaglandin F2α (PGF) as a major embryotoxic factor during early embryonic development in cattle. Elevated uterine concentrations of PGF were negatively associated with embryo development, quality and pregnancy rates (Schrick FN et al. 1993 Biol. Reprod. 49, 617–621; Hockett ME et al. 1998 J. Anim. Sci. 76 (Suppl 1), 241 abst; Seals RC et al. 1998 Prostaglandins 56, 377–389). Moreover, addition of PGF to culture medium decreased hatching rates of compacted morulae (Scenna FN et al. 2002 Theriogenology 53, 512 abst) and decreased development of pre-compacted (16–32 cell) bovine embryos to blastocyst stage (Scenna FN et al. 2003 Theriogenology 59, 335 abst). Furthermore, administration of an inhibitor of PGF synthesis at the time of embryo transfer improved pregnancy rates in cattle (Schrick FN et al. 2001 Theriogenology 55, 370 abst). The objective of the current study was to identify the period of time during early embryonic development that is most susceptible to the deleterious effects of PGF. After in vitro maturation and fertilization of bovine oocytes, putative zygotes were cultured in KSOMaa plus 0.3% BSA. On Day 4 post-insemination, pre-compacted (16–32 cell) embryos were removed from culture, evaluated for quality, and randomly assigned to one of the following treatments: 1) Control (KSOMaa plus 0.3% polyvinyl alcohol (KSOM-PVA; n=470) or 2) PGF-1 (1ngmL−1 PGF in KSOM-PVA; n=473; Scenna FN et al. 2003 Theriogenology 59, 335 abst). After 48h of incubation in assigned treatments, assessment of development to compacted morula stage was determined. Thereafter, embryos were kept separate according to treatments, sorted by stage of development and quality, and randomly assigned to receive either Control (CON) or PGF-1 supplemented medium until assessment of blastocyst development on Day 9. This random sorting resulted in the formation of four treatment groups comprising the initial treatments and assigned treatments during Days 6–9 (CON-CON, n=366; PGF-CON, n=226; CON-PGF, n=149; PGF-PGF, n=287). Analyses were performed incorporating a randomized incomplete block design using mixed models of SAS (2000) to determine effects of PGF on Days 4–6, 6–9 and 4–9 of development. Data were also analyzed using chi-square. Addition of 1ngmL−1 of PGF to culture medium on Days 4–9 decreased the percentage of pre-compacted embryos reaching blastocyst stage (CON-CON, 47.8%; PGF-PGF, 36%; P&lt;0.05). Moreover, addition of 1ngmL−1 of PGF to the culture medium of pre-compacted bovine embryos on Days 4–6 of development decreased the percentage of compacted morulae on Day 6 (Control, 68.1%; PGF-1, 60.5%; P=0.01). However, the percentage of embryos developing to blastocyst was not decreased following addition of 1ngmL−1 of PGF on Days 6–9 of development (CON-CON, 47.8%; CON-PGF, 42.6%; P&gt;0.05). Results suggest that morula stage embryos during compaction are most susceptible to deleterious effects of PGF.


2012 ◽  
Vol 36 (2) ◽  
pp. 272 ◽  
Author(s):  
Jie TAN ◽  
Hui-ling SUN ◽  
Fei GAO ◽  
Jing-ping YAN ◽  
Ying-hui DONG ◽  
...  

2010 ◽  
Vol 34 (5) ◽  
pp. 777-785 ◽  
Author(s):  
Wei SONG ◽  
Jia-kun SONG ◽  
Chun-xin FAN ◽  
Tao ZHANG ◽  
Bin WANG

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Aslı Okan ◽  
Necdet Demir ◽  
Berna Sozen

AbstractDiabetes mellitus (DM) has profound effects on the female mammalian reproductive system, and early embryonic development, reducing female reproductive outcomes and inducing developmental programming in utero. However, the underlying cellular and molecular mechanisms remain poorly defined. Accumulating evidence implicates endoplasmic reticulum (ER)-stress with maternal DM associated pathophysiology. Yet the direct pathologies and causal events leading to ovarian dysfunction and altered early embryonic development have not been determined. Here, using an in vivo mouse model of Type 1 DM and in vitro hyperglycaemia-exposure, we demonstrate the activation of ER-stress within adult ovarian tissue and pre-implantation embryos. In diabetic ovaries, we show that the unfolded protein response (UPR) triggers an apoptotic cascade by the co-activation of Caspase 12 and Cleaved Caspase 3 transducers. Whereas DM-exposed early embryos display differential ER-associated responses; by activating Chop in within embryonic precursors and Caspase 12 within placental precursors. Our results offer new insights for understanding the pathological effects of DM on mammalian ovarian function and early embryo development, providing new evidence of its mechanistic link with ER-stress in mice.


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