Regulation of functional and regressing stages of corpus luteum development in mice. Role of reactive oxygen species
Valeria A. Sander A , Lidia Piehl B , Graciela B. Facorro B , Emilio Rubín de Celis B and Alicia B. Motta A CA Laboratorio de Fisiopatología Ovárica – Centro de Estudios Farmacológicos y Botánicos (CEFYBO), Consejo Nacional de Investigaciones Científicas y Tecnológicas (CONICET)/ Departamento de Farmacología, Facultad de Medicina, Universidad de Buenos Aires, Buenos Aires, Argentina.
B Cátedra de Física, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Buenos Aires, Argentina.
C Corresponding author. Email: aliciabmotta@yahoo.com.ar
Reproduction, Fertility and Development 20(7) 760-769 https://doi.org/10.1071/RD08051
Submitted: 15 March 2008 Accepted: 15 June 2008 Published: 1 August 2008
Abstract
The endocrine and immune systems modulate ovarian function. The aim of the present work was to compare the status of various modulating factors in two well-defined stages of corpus luteum (CL) development (the functional stage and the regressing stage) by means of a gonadotropin-synchronised mouse model. At the regressing stage of CL development, we found that ovarian tissue showed increased prostaglandin (PG) F2α and diminished PGE levels concomitantly with enhanced protein abundance of ovarian cyclooxygenase 2, the inducible isoform of the limiting enzyme of PG synthesis. We also found both enhanced lipid peroxidation and enhanced total superoxide dismutase activity, as well as inhibited catalase activity and inhibited total hydroxyl radical scavenger capacity, when compared with ovaries at the functional stage. In addition, at the regressing stage we observed an increased percentage of CD8+ (cytotoxic/suppressor) T-cells and a decreased percentage of CD4+ (helper) T-cells from ovarian-draining lymph nodes. Also, the serum interleukin (IL)-2, IL-4 and IL-10 were diminished as compared with the functional stage. We conclude that a pro-oxidant status together with a pro-inflammatory response is responsible for the loss of luteal function.
Additional keywords: cytokines, luteal regression, oxidative stress.
Acknowledgements
This work was supported by PIP CONICET Ref 6051 from Consejo Nacional de Investigaciones Científicas y Tecnológicas, PICTR 32529 and PICT 949 from Agencia Nacional de Promoción Científica y Tecnológica. We thank Dr Marta Dubin, Dr Elida Gonzalez, Lic. Maria Emilia Solano, Lic. Carolina Luchetti and Lic. Evelin Elia for their invaluable help.
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