Open Access

ARTICLE

Preimplantation embryotoxicity after mouse embryo exposition to reactive oxygen species

ELISA CEBRAL^1,2, ISABEL CARRASCO¹ , DAVID VANTMAN¹, ROSITA SMITH¹

1. Instituto de Investigaciones Materno-Infantil, Hospital Clínico Materno-Infantil San Borja-Arriarán, Facultad de Medicina, Universidad de Chile. Santa Rosa 1234, Santiago, Chile.
2. Laboratorio de Biología del Desarrollo, Instituto de Fisiología, Biología Molecular y Neurociencias (IFIBYNE-CONICET), Pabellón II, 4to. Piso, Ciudad Universitaria, Capital Federal, Buenos Aires, Argentina. Centro de Estudios Farmacológicos y Botánicos (CEFYBO-CONICET). Paraguay 2155, piso 16. Capital Federal, Buenos Aires, Argentina.
Address correspondence to: Dra. Elisa Cebral. IFIBYNECONICET / DBBE-FCEN. Lab. 15-21, 4to Piso, Pab.II. Ciudad Universitaria, (CP 1428) Capital Federal, Buenos Aires, ARGENTINA. Phone: (+54-11) 4576 3300. E-mail: ecebral@hotmail.com

BIOCELL 2007, 31(1), 51-59. https://doi.org/10.32604/biocell.2007.31.051

Abstract

Exposure of either gametes or embryos to conditions and/or factors that generate oxidative stress has been associated with impaired early embryogenesis. The effects of reactive oxygen species (ROS) on mouse preimplantation development, depending of the ROS-concentration and time of exposition, were studied. Two-cell embryos were incubated with 5, 10, 25 and 50 μM of hydrogen peroxide (H₂O₂) for 30 and 60 minutes of exposition and allowed to develop for 72 h to study the quality of development. The incubation with 50 μM H₂O₂ for 30 or 60 minutes, strongly inhibited the 2-cell embryo development as compared to the control (p<0.001). Twenty-five μM H₂O₂ produced inhibition of blastocyst formation (p<0.001) and 10 μM H₂O₂ significantly decreased the percentages of expanded and hatched blastocysts, which resulted morphologically altered (p<0.05 and p<0.01, respectively). The higher H₂O₂ concentrations were able to elicit necrotic morphology in the 2-cell arrested embryos, while 10 μM H₂O₂ induced moderate damage with the arrested embryos partially fragmented. In conclusion, important causes for defective preimplantation development and for early embryo losses may be due to oxidative stress because early mouse embryos exposed to ROS for short times arrested at the first cellular cycle (2-cell) and/or impaired embryo differentiation and morphogenesis, being these effects ROS-concentration-dependent.

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