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AJP - Endocrinology and Metabolism, Vol 256, Issue 6 E753-E759, Copyright © 1989 by American Physiological Society
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L. L. Espey, N. Tanaka and H. Okamura
Department of Biology, Trinity University, San Antonio, Texas 78284.
The ovulatory process was initiated in 25-day-old Wistar rats by injecting human chorionic gonadotropin (hCG; 10 IU sc) 2 days after the animals had been primed with pregnant mares serum gonadotropin (PMSG; 10 IU sc). By 4 h into the ovulatory process, leukotriene (LT) B4 increased 2-fold (P less than 0.001) and LTs C4/D4/E4 increased 1.3-fold (P less than 0.002). By the time of ovulation (10-12 h after the administration of hCG) both eicosanoids declined to their pre-hCG levels. When animals were treated with the cyclooxygenase inhibitor indomethacin at the specific dose of 0.316 mg/rat sc at 1 h before hCG, the ovarian levels of LT B4 and LTs C4/D4/E4 increased to 210% (P less than 0.01) and 113% (P less than 0.05), respectively, above the control levels at 4 h after hCG. Concomitantly, this dosage of indomethacin reduced ovarian prostaglandins (PGs) E and F by 99% (P less than 0.001) and 98% (P less than 0.001), respectively, and it reduced the ovulation rate by 76% (P less than 0.001). Thus it appears this dose of indomethacin blocked the conversion of ovarian arachidonic acid into PGs and shunted this substrate into the lipoxygenase pathways that lead to LT formation. In conclusion, the moderate increase in ovarian LTs is characteristic of inflammatory reactions, and, therefore, these data support the hypothesis that the biochemical events of ovulation resemble an inflammatory process.
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