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Nitric oxide modulates mitochondrial activity and apoptosis through protein S-nitrosylation for preimplantation embryo development.
Lee, Tsung-Hsien; Lee, Maw-Sheng; Huang, Chun-Chia; Tsao, Hui-Mei; Lin, Pi-Mei; Ho, Hong-Nerng; Shew, Jin-Yuh; Yang, Yu-Shih.
Afiliação
  • Lee TH; Department of Obstetrics and Gynecology, National Taiwan University and National Taiwan University Hospital, #8 Chung-Shan South Road, 100, Taipei, Taiwan.
J Assist Reprod Genet ; 30(8): 1063-72, 2013 Aug.
Article em En | MEDLINE | ID: mdl-23832270
PURPOSE: Previous studies reported that patients with endometriosis had excess nitric oxide (NO) in the reproductive tract and poor embryo development in IVF cycles. This study aims to elucidate the effects of NO on early embryo development. METHODS: Zygotes from superovulated B6CBF1 mice were cultured to blastocysts in a variety of media. Sodium nitroprusside (SNP) and N(G)-nitro-L-arginine (LNA) were added to the culture medium as a NO donor and a NO synthase inhibitor, respectively. The localization and fluorescence intensity of S-nitrosylated (SNO) proteins within 2-cell stage embryos were analyzed with confocal microscopy. Apoptosis and ATP production in the blastocysts were measured. RESULT(S): Subsequent to NO exposure, the SNO proteins mainly colocalized with the mitochondria and endoplasmic reticulum and the intensity of SNO proteins increased. The addition of a quanylate cyclase inhibitor and a cyclic GMP mimic agent induced nonsignificant changes in SNO proteins, whereas addition of a superoxide scavenger or a reduced form of glutathione rescued the embryos from the effects of NO. However, superoxide scavenger supplementation resulted in decreased blastocyst ATP production. CONCLUSION(S): Elevated NO exerts deleterious effects on embryo development, possibly through protein S-nitrosylation in the mitochondria and endoplasmic reticulum. Including glutathione as a component in the culture medium might counteract this effect.
Assuntos

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Blastocisto / Apoptose / Desenvolvimento Embrionário / Mitocôndrias / Óxido Nítrico Limite: Animals Idioma: En Revista: J Assist Reprod Genet Assunto da revista: GENETICA / MEDICINA REPRODUTIVA Ano de publicação: 2013 Tipo de documento: Article País de afiliação: Taiwan

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Blastocisto / Apoptose / Desenvolvimento Embrionário / Mitocôndrias / Óxido Nítrico Limite: Animals Idioma: En Revista: J Assist Reprod Genet Assunto da revista: GENETICA / MEDICINA REPRODUTIVA Ano de publicação: 2013 Tipo de documento: Article País de afiliação: Taiwan