Ubiquinol-10 delays postovulatory oocyte aging by improving mitochondrial renewal in pigs

Abstract

Ubiquinol-10, the reduced form of coenzyme Q10, protects mammalian cells from oxidative damage and enhances mitochondrial activity. However, the protective effect of ubiquinol-10 on mammalian oocytes is not well understood. In this study, we investigated the effect of ubiquinol-10 on porcine oocytes during postovulatory aging. Metaphase II oocytes were selected as fresh oocytes and further cultured for 48 h with different concentrations of ubiquinol-10 (0-400 μM) in vitro as a postovulatory aging model. After choosing the optimal concentration of ubiquinol-10 (100 μM) that maintained oocyte morphology and developmental competence during the progression of aging, the oocytes were randomly divided into five groups: fresh, control-24 h, ubiquinol-24 h, control-48 h, and ubiquinol-48 h. The results revealed that ubiquinol-10 significantly prevented aging-induced oxidative stress, GSH reduction, cytoskeleton impairment, apoptosis, and autophagy. Mitochondrial biogenesis (SIRT1 and PGC-1α) and mitophagy (PINK1 and PARKIN)-related proteins were decreased during aging. Addition of ubiquinol-10 prevented the aging-induced reduction of these proteins. Consequently, although mitochondrial content was decreased, the number of active mitochondria and ATP level were significantly increased upon treatment with ubiquinol-10. Thus, ubiquinol-10 has beneficial effects on porcine postovulatory aging oocytes owing to its antioxidant properties and ability to promote mitochondrial renewal.

Inhibitory effects of astaxanthin on postovulatory porcine oocyte aging in vitro

“…The spindle as an important structure for accurate chromosomal distribution, is correlated with coordination interaction between the actin and microtubule cytoskeleton. The aged oocytes often present with spindle disruption and actin reduction 55 . In the present study, Ax treatment attenuated the spindle abnormality and restored the actin expression for aged oocytes, indicating its protection on cytoskeletal stability.…”

Imperatorin Ameliorates the Aging-Associated Porcine Oocyte Meiotic Spindle Defects by Reducing Oxidative Stress and Protecting Mitochondrial Function

“…The up-regulated mRNA expression of GDF9, BMP15, MOS, and CCNB1 suggested that IMP might be involved in regulating oocyte cytoplasmic maturation ( Su et al, 2004 ; De Castro et al, 2016 ; Liu et al, 2018 ), as well as promoting MPF activity ( Peter et al, 2002 ; Madgwick and Jones, 2007 ; Yang et al, 2017 ). Moreover, stable MOS and CCNB1 levels are essential for meiosis mediated by MAD1, MPS1, and APC/C Cdc 20 ( Alfonso-Pérez et al, 2019 ), as well as balancing the MAPK, NF-κB signal which affects the ROS and mitochondrial dysfunction-mediated oocyte aging ( Achache et al, 2020 ; Niu et al, 2020 ; Zhu et al, 2020 ). In addition, relatively high levels of GDF9 and BMP15 also help slow down the aging and reduce the apoptosis of oocytes by luteinizing hormone receptor, BCL2/BAX, connexin43-mediated regulating the steroidogenic acute regulatory protein expression, plasminogen activator, gap junctions ( Hussein et al, 2005 ; Chang et al, 2014 ; De Castro et al, 2016 ).…”

“…Spindles and actin filaments of oocyte are sensitive to chemicals and aging ( Sun and Kim, 2012 ; Liang et al, 2018 ; Niu et al, 2020 ). Our results showed that the rate of abnormal spindle morphology in aged oocytes exposed to 40 μM IMP is markedly lower than that in control oocytes.…”

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“…Spindles and actin filaments of oocyte are sensitive to chemicals and aging (Sun and Kim, 2012;Liang et al, 2018;Niu et al, 2020). Our results showed that the rate of abnormal spindle morphology in aged oocytes exposed to 40 µM IMP is markedly lower than that in control oocytes.…”

“…affects the ROS and mitochondrial dysfunction-mediated oocyte aging (Achache et al, 2020;Niu et al, 2020;Zhu et al, 2020). In addition, relatively high levels of GDF9 and BMP15 also help slow down the aging and reduce the apoptosis of oocytes by luteinizing hormone receptor, BCL2/BAX, connexin43-mediated regulating the steroidogenic acute regulatory protein expression, plasminogen activator, gap junctions (Hussein et al, 2005;Chang et al, 2014;De Castro et al, 2016).…”