비밀번호 확인 :
Konkuk Research Team identifies cytotoxic effects of Dimethyl sulfoxide in mouse pre-implementation embryos
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2017.11.01
<div style="text-align: justify;"> <p>A research team led by Professor Jin-Hoi Kim of the Department of Stem Cell and Regenerative Biotechnology, Humanized Pig Research Center (SRC), has found that Dimethyl sulfoxide (DMSO) supplementation induces long-term negative effects on pre-implantation embryo development for the first time.<br /><br /><br /></p> <br /><span style="font-family: arial,helvetica,sans-serif; font-size: 10pt;"><img alt="" src="ArticleFile.do?id=11713589" /></span></div> <div style="text-align: justify;"> <p><br />On October 17, 2017, the research, named “The cytotoxic effects of dimethyl sulfoxide in mouse preimplantation embryos: a mechanistic study” which was supported by the Science Research Center of the National Research Foundation of Korea, was published in <em>Theranostics,</em> an open access journal for the integration of therapeutics and diagnostics.<br /><br /><span style="font-family: arial,helvetica,sans-serif; font-size: 10pt;"><img alt="" src="ArticleFile.do?id=11713593" /><img width="768" height="543" alt="" src="ArticleFile.do?id=11713592" /></span></p> </div> <div style="text-align: justify;"> <p>Dimethyl sulfoxide (DMSO) is commonly used as a solvent for water-insoluble substances, a vehicle for drug therapy, and a cryoprotectant for cultured cells. It is frequently used in a wide range of biological studies, and its function has been investigated in various contexts. However, its molecular mechanisms have not been clearly defined.</p> </div> <div style="text-align: justify;"> <p>Professor Kim’s research team found out exposure to DMSO induces an early oxidative stress response within 0.5 to 2 h in 1-cell zygotes by disrupting the balance of pro- and anti-oxidants. Notably, DMSO-treated 2-cell embryos shows increased expression of unfolded protein response genes such as <em>Hspa5, Hsp90b1, Ddit3, Atf4,</em> and <em>Xbp1</em>. As a result, the development of many embryos is arrested at the 2-cell, 4-cell, or morula stages in a dose-dependent manner. Further, DMSO-induced endoplasmic reticulum stress increases mitochondrial Ca<sup>2+</sup> levels, induces mitochondrial depolarization/dysfunction, and induces apoptotic cell death via the JNK/ATF2-dependent pathway. Consequently, treatment with DMSO increases the expression of autophagy initiation-, phagophore elongation-, and autophagosome formation-related genes, as well as localization of PINK1/Parkin, which are the main mediators of mitophagy, in mitochondria. Interestingly, DMSO causes cytotoxic effects in preimplantation embryos by inducing extensive mitophagy and autophagy. Especially, DMSO treatment decreases the inner cell mass and trophectoderm cell numbers as well as mRNA expression of <em>B3gnt5</em> and <em>Wnt3a</em> in developed blastocysts, which decreases the implantation and developmental rates of full-term offspring after being transferred into pseudopregnant mice.</p> <p>“The research result is of high scientific value for it can partially explain the cause of frequently occurring side effects of DMSO which is most widely used in biological and medical experiments. Due to its severe side effects, it is unavoidable for academia to partially modify the current practices using DMSO as a control group,” said Professor Kim.</p> </div>
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