Search

Arsenic (AS), an environmental contaminant, is a known human carcinogen that can cause cancer of the lung, liver, and skin. Furthermore, AS induces oxidative stress and mitochondrial impairments in mammalian cells. However, limited information is available on the effect of AS exposure on oocyte maturation of porcine, whose anatomy, physiology, and metabolism are similar to those of human. Therefore, we examined the effect of AS exposure on the in vitro maturation (IVM) of porcine oocytes and the possible underlying mechanisms. Cumulus-cell enclosed oocytes were cultured with or without AS for maturation, and then were used for analyses. This study indicated that AS under a concentration of 1 μM significantly increased the abnormal expansion of cumulus cells and the number of oocytes maintained in meiotic arrest. In addition, AS exposure significantly reduced subsequent development of embryos and increased the rate of apoptosis of blastocysts following parthenogenetic activation (PA) and in vitro fertilization (IVF). Moreover, AS exposure induced oxidative stress with increased reactive oxygen species (ROS), and decreased glutathione (GSH), leading to reduced mitochondrial membrane potential, mitochondrial quantity, DNA damage, excessive autophagy activity, and early apoptosis in porcine oocytes. Taken together, the results demonstrated that AS exposure exerts several negative effects, such as meiotic defects and embryo developmental arrest by causing mitochondrial dysfunction and apoptosis via inducing oxidative stress., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 The Authors. Published by Elsevier B.V. All rights reserved.)

Heat stress (HS) is an emerging issue that greatly impairs the reproductive performance of animals and humans. In particular, disruption of oocyte maturation due to HS is considered a major cause of impaired reproductive performance. HS is known to induce ceramide generation, which causes reactive oxygen species (ROS) production and mitochondrial dysfunction, thereby inducing apoptosis. Therefore, we investigated whether inhibition of ceramide generation ameliorates HS-induced apoptosis in porcine cumulus-oocyte complexes (COCs) using specific inhibitors of the de novo (fumonisin B1, FB1) and hydrolytic pathways (desipramine, Des) of ceramide formation. We investigated the effects of FB1 and Des supplementation under HS conditions (41.5 °C for 44 h) on in vitro maturation (IVM) of porcine COCs. After IVM, HS significantly reduced proportion of COCs exhibiting fully expanded cumulus cells and the rate of metaphase II in oocytes. After parthenogenetic activation (PA), HS significantly reduced the rates of cleavage and blastocyst formation with a lower total cell number and a higher percentage of apoptosis in blastocysts. However, FB1 or Des supplementation under HS avoided detrimental effects of HS on expansion of cumulus cells, nuclear maturation of oocytes, and embryonic development after PA including the rates of cleavage and blastocyst formation, total cell number, and the percentage of apoptosis in blastocysts. Furthermore, FB1 or Des addition under HS, compared with HS alone, significantly decreased ceramide generation, ROS production, cytochrome C expression, and apoptosis and increased mitochondrial membrane potential in COCs, reaching levels comparable with those of the control. Taken together, our results indicate that HS impaired oocyte maturation through ceramide-mediated apoptosis., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020 Elsevier B.V. All rights reserved.)