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Human Reproduction, Vol. 15, No. 12, 2512-2519, December 2000
© 2000 European Society of Human Reproduction and Embryology

GnRH agonist-suppressed expression of nitric oxide synthases and generation of peroxynitrite in adenomyosis

Yasuhiko Kamada, Mikiya Nakatsuka1, Kazuo Asagiri, Soichi Noguchi, Toshihiro Habara, Masayo Takata and Takafumi Kudo

Department of Obstetrics and Gynecology, Okayama University Medical School, Okayama-city, Okayama, Japan

Because overproduction of nitric oxide (NO) and peroxynitrite is known to cause tissue injury, the expression of NO synthases (NOS) and generation of peroxynitrite were investigated in adenomyosis. Immunoreactivities to endothelial and inducible NOS demonstrated phase-dependent changes in normal endometrium, and in eutopic endometrium of adenomyosis. However, NOS were expressed throughout the menstrual cycle in ectopic endometrium from the majority of patients with adenomyosis. Nitrotyrosine, a footprint of peroxynitrite, was detected concomitantly with NOS protein. This suggested that high doses of NO and superoxide are produced in the ectopic endometrium, presumably by stimulation with bioactive molecules such as cytokines and growth factors. The expression of NOS and generation of peroxynitrite were markedly reduced by administration of gonadotrophin-releasing hormone agonists (GnRHa). The suppression of serum concentrations of nitrite/nitrate, stable metabolites of NO, by long-term administration of GnRHa was also demonstrated. The suppression of synthesis of NO and/or peroxynitrite may be part of both the therapeutic and adverse effects of GnRHa therapy.

Key words: adenomyosis/GnRH agonist/nitric oxide/peroxynitrite

1 To whom correspondence should be addressed at: Department of Obstetrics and Gynecology, Okayama University Medical School, 2-5-1 Shikata, Okayama-City, Okayama, 700-8558, Japan.E-mail: mikiya{at}cc.okayama-u.ac.jp


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