title: Mdivi-1, mitochondrial fission inhibitor, impairs developmental competence and mitochondrial function of embryos and cells in pigs.
abstract: Mitochondria are highly dynamic organelles that undergo constant fusion/fission as well as activities orchestrated by large dynamin-related GTPases. These dynamic mitochondrial processes influence mitochondrial morphology, size and function. Therefore, this study was conducted to evaluate the effects of mitochondrial fission inhibitor, mdivi-1, on developmental competence and mitochondrial function of porcine embryos and primary cells. Presumptive porcine embryos were cultured in PZM-3 medium supplemented with mdivi-1 (0, 10 and 50 μM) for 6 days. Porcine fibroblast cells were cultured in growth medium with mdivi-1 (0 and 50 μM) for 2 days. Our results showed that the rate of blastocyst production and cell growth in the mdivi-1 (50 μM) treated group was lower than that of the control group (P < 0.05). Moreover, loss of mitochondrial membrane potential in the mdivi-1 (50 μM) treated group was increased relative to the control group (P < 0.05). Subsequent evaluation revealed that the intracellular levels of reactive oxygen species (ROS) and the apoptotic index were increased by mdivi-1 (50 μM) treatment (P < 0.05). Finally, the expression of mitochondrial fission-related protein (Drp 1) was lower in the embryos and cells in the mdivi-1-treated group than the control group. Taken together, these results indicate that mdivi-1 treatment may inhibit developmental competence and mitochondrial function in porcine embryos and primary cells.
authors.affiliation: Department of Biotechnology, College of Engineering, Daegu University, Gyeongbuk 712-714, Republic of Korea.
authors.forename: Ji-Yeong
authors.initials: JY
authors.lastname: Yeon
authors.forename: Sung-Hun
authors.initials: SH
authors.lastname: Min
authors.forename: Hyo-Jin
authors.initials: HJ
authors.lastname: Park
authors.forename: Jin-Woo
authors.initials: JW
authors.lastname: Kim
authors.forename: Yong-Hee
authors.initials: YH
authors.lastname: Lee
authors.forename: Soo-Yong
authors.initials: SY
authors.lastname: Park
authors.forename: Pil-Soo
authors.initials: PS
authors.lastname: Jeong
authors.forename: Humdai
authors.initials: H
authors.lastname: Park
authors.forename: Dong-Seok
authors.initials: DS
authors.lastname: Lee
authors.forename: Sun-Uk
authors.initials: SU
authors.lastname: Kim
authors.forename: Kyu-Tae
authors.initials: KT
authors.lastname: Chang
authors.forename: Deog-Bon
authors.initials: DB
authors.lastname: Koo
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects* / Q000502:physiology; D064550:Death-Associated Protein Kinases / Q000378:metabolism; D046149:Embryo Culture Techniques; D047108:Embryonic Development / Q000187:drug effects* / Q000502:physiology; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects* / Q000502:physiology; D008928:Mitochondria / Q000187:drug effects* / Q000378:metabolism; D063154:Mitochondrial Dynamics / Q000187:drug effects / Q000502:physiology; D052999:Quinazolinones / Q000494:pharmacology*; D017382:Reactive Oxygen Species / Q000378:metabolism; D013552:Swine
chemical_list: C549041:3-(2,4-dichloro-5-methoxyphenyl)-2-sulfanyl-4(3H)-quinazolinone; D052999:Quinazolinones; D017382:Reactive Oxygen Species; D064550:Death-Associated Protein Kinases