dinoprost and 3-4-3--4--tetrachlorobiphenyl

Polychlorinated biphenyls (PCBs) stimulate in vitro both the force of myometrial contractions and endometrial secretion of PGF2alpha in cattle. Therefore, the goal of this study was to investigate the participation of PGF2alpha in the effect of PCBs on uterine contractility. For this aim, the myometrial strips were incubated (48h) with PCB 77 at the dose of 1, 10 and 100ng/ml (i.e., 0.0034, 0.034 and 0.34nmol/ml) separately or jointly with indomethacin (INDO, 10(-4)M), which blocks the PGF2alpha synthesis. Next, the force of myometrial strips contractions was measured. Further, the influence of PCB 77 (0.1, 1 and 10ng/ml) on the PGF2alpha secretion from myometrial cells after 6, 24, and 48h and PCB 77 (1 and 10ng/ml) on the mRNA expression of cyclooxygenase 2 (COX-2) and PGF2alpha synthase (PGFS) in myometrial cells after 6 and 24h, was investigated. The increase (P<0.05-0.001) of the contractions force of myometrial strips evoked by each dose of PCB 77, was markedly reduced (P<0.05-001) by INDO. There was an increase (P<0.05-0.001) of both PGF2alpha secretion after all studied periods of cell incubation and mRNA expression for COX-2 and PGFS after 6h treatment of myometrial cells with PCB 77. It can be concluded that myometrial synthesis of PGF2alpha and its further secretion is a part of the mechanism by means of which PCB 77 may affect the force of myometrial contractions in cattle.

Topics: Animals; Cattle; Cyclooxygenase 2; Dinoprost; Dose-Response Relationship, Drug; Female; Gene Expression Regulation, Enzymologic; Hydroxyprostaglandin Dehydrogenases; Indomethacin; Myometrium; Polychlorinated Biphenyls; RNA, Messenger; Time Factors; Uterine Contraction

Exposure of chick embryos in ovo to cytochrome P-448 inducers 2,3,7,8-tetrachlorodibenzo-p-dioxin, 3,4,3',4'-tetrachlorobiphenyl, 3,4,5,3',4',5'-hexachlorobiphenyl and beta-napthoflavone, increased cardiac prostaglandins in vitro. The dose response relationships were biphasic with prostaglandin release increasing at the low doses and returning to basal levels at higher doses. Phenobarbital was ineffective. Increased cardiac prostaglandin release was detected at doses that induced hepatic 7-ethoxyresorufin deethylase (7-ER) but which were below the threshold for cardiac induction. The fall in prostaglandin release coincided with induction of cardiac 7-ER and therefore may be attributable to increased prostaglandin metabolism. These studies show that the P-450 system may interact with the arachidonic acid metabolizing system to increase PG release and that this effect may be part of the pleiotypic response to Ah-receptor activation.

Topics: 6-Ketoprostaglandin F1 alpha; Animals; Benzoflavones; beta-Naphthoflavone; Calcimycin; Chick Embryo; Cytochrome P-450 CYP1A1; Cytochrome P-450 CYP1A2; Cytochromes; Dinoprost; Dinoprostone; Dioxins; Enzyme Induction; Heart; Liver; Myocardium; Oxidoreductases; Polychlorinated Biphenyls; Polychlorinated Dibenzodioxins; Prostaglandins E; Prostaglandins F; Thromboxane B2