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Department of Obstetrics and Gynecology, Fujita-Gakuen Health University School of Medicine Aichi
the Department of Obstetrics and Gynecology, Tokyo Dental College, Ichikawa General Hospital (T.O.) Chiba
the Department of Obstetrics and Gynecology, Kyorin University School of Medicine (Y.N.) Tokyo, Japan
Address requests for reprints to: Yasunori Yoshimura, M.D., Department of Obstetrics and Gynecology, Fujita-Gakuen Health University School of Medicine, 1–98 Dengakugakubo, Kutsukake, Toyoake City, Aichi, Japan 470–11.
The present study was undertaken to assess the effects of the products of the lipoxygenase pathway on steroi-dogenesis and the production of prostaglandins (PGs) by human corpora lutea in the midluteal phase. In the first experiment luteal cells were cultured with 5-hydroxyeicosatetraenoic acid (5-HETE) at 10, 100, 500, or 1000 ng/mL in the presence or absence of hCG at 100 ng/mL for 10 days. The addition of 5-HETE dose-dependently inhibited progesterone (P) production by the cultured luteal cells. P production stimulated by exposure t o hCG was also reduced significantly in response to 5-HETE. However, 5-HETE had no effect on the production of 6-keto-PGF1
, PGF2
, or PGE2 by cultured luteal cells at any point during the culture period. In the second experiment the reaction products of soybean lipoxidase of arachidonic acid (AA-LIP) were added to cultured luteal cells. Treatment with either AA or LIP alone had no effect on basal P production. The addition of AA-LIP at all concentrations tested reduced P production by cultured luteal cells in the presence or absence of hCG. AA-LIP significantly reduced basal 6-keto-PGF1
secretion in cultured luteal cells on day 2. Although the stimulatory effect of AA on luteal PGE2 production was maintained throughout the entire culture period, the lipoxygenase products of AA did not affect AA-stimulated PGE2 production by cultured luteal cell. These results suggest that the products of the lipoxygenase pathway may be important in the involution of human corpora lutea.
Received July 27, 1989.
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