Effects of Tumor Necrosis Factor-α and Nitric Oxide on Prostaglandins Secretion by the Bovine Oviduct Differ in the Isthmus and Ampulla and Depend on the Phase of the Estrous Cycle

Author:

Siemieniuch Marta J.1,Woclawek-Potocka Izabela1,Deptula Katarzyna1,Okuda Kiyoshi1,Skarzynski Dariusz J.1

Affiliation:

1. Department of Reproductive Immunology and Pathology, Institute of Animal Reproduction and Food Research of the Polish Academy of Sciences, 10-747 Olsztyn, Poland; and Graduate School of Natural Science and Technology, Okayama University, Tsushima Naka, 700-8530, Japan

Abstract

To determine the possible roles of tumor necrosis factor-α (TNFα) and nitric oxide (NO) in the bovine oviduct, ampulla and isthmus collected during the estrous cycle were exposed for 18 h to TNFα, NO donor (NONOate), NO synthase inhibitors (L-NOARG, L-NAME and AMT) and oxytocin (OT) as a positive control. Prostaglandins (PGs) and NO2/NO3 in conditioned media were measured. TNFα stimulated PGF secretion on Day 0 (onset of estrus = Day 0) and Days 2–3, in both the ampulla and isthmus, but on Days 18–20 only in ampulla. TNFα increased PGE2 secretion in both fragments in each phase. NONOate did not affect PGF secretion on Days 18–20, whereas this NO donor stimulated PGF secretion in both fragments on Day 0 and Days 2–3. TNFα increased NO2/NO3 production in every examined phase in the ampulla and on Days 2–3 in the isthmus. L-NAME lowered NO2/NO3 production regardless of phase or fragment. L-NOARG and AMT lowered NO2/NO3 production in both fragments on Day 0 and Days 2–3. The possible role of TNFα, NO or PGs on the oviductal contractility during the early-luteal phase was also examined. Neither TNFα nor NONOate influenced contractility in either fragment. Although PGF stimulated the contraction in both fragments, PGE2 decreased it. When taken together, TNFα seems to play some role as a modulator of PGF and PGE2 production and for transferring the embryo from the oviduct to the uterus by stimulating NO production in the bovine oviduct.

Publisher

SAGE Publications

Subject

General Biochemistry, Genetics and Molecular Biology

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