6-ketoprostaglandin-f1-alpha and 3-4-3--4--tetrachlorobiphenyl

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