ENHANCED INACTIVATION OF PROSTAGLANDIN E 2 BY THE RABBIT LUNG DURING PREGNANCY OR PROGESTERONE TREATMENT

One to 7 days after whole body exposure of mice to a single dose of 700 R of x‐rays, little or no change was detected in prostaglandin‐like activity in the brain, blood and seminal vesicles. Slight increases in intestinal and renal tissue were not significant. In the lung, mean activity rose from 62 ng/g to a transient peak of 145 ng/g wet weight on the fourth day (P > 0.05). In the spleen, mean levels rose steadily from 13.2 ng/g to 259 ng/g on the fourth day (P < 0.01), and were still 184.4 ng/g on the seventh day. Prostaglandin‐like activity was measured 4 days after single doses of 200–700 R. In the lung, a significant rise was produced by 600 and 700 R, and in the spleen by 200–700 R. Thin layer chromatography showed that part of the prostaglandin‐like activity in spleen extracts had an RF similar to that of [3H]‐prostaglandin E1, and part to that of [3H]‐prostaglandin F2α. Splenic tissue from mice exposed to 700 R four days earlier, inactivated prostaglandin E1 less potently than did tissue from non‐irradiated mice.

Section: Methodsmentioning

confidence: 99%

Effect of Ionizing Radiation on Prostaglandin‐like Activity in Tissues

Eisen

Walker

1976

“…The method used to determine the pulmonary inactivation of prostaglandin E2 is a modification of that of Horton & Jones (1969) and has been used by other workers (Ueda, Hatanaka, Ito, Kokubu & Hamamura, 1973;Bedwani & Marley, 1974). It assumes that the depressor effects of prostaglandin E2 are due solely to peripheral vasodilatation.…”

Section: Discussionmentioning

confidence: 99%

INHIBITION OF THE PULMONARY INACTIVATION OF PROSTAGLANDINS in vivo BY DI‐4‐PHLORETIN PHOSPHATE

Crutchley

Piper

1975

1Inactivation of prostaglandin E2 in the pulmonary circulation of rabbits in vivo was measured by comparing the hypotensive effects of doses given intravenously and intra-arterially.2 Di-4-phloretin phosphate (DPP) 25-100l,g kg-l min-' inhibited the inactivation of prostaglandin E2 in the pulmonary circulation. 3 These doses of DPP caused a marked shift to the left of the dose-response curve to prostaglandin E2 given intravenously but did not affect the dose-response curve to prostaglandin F2 given intra-arterially. 4 Inhibition of pulmonary inactivation of prostaglandins E2 and F 2, caused marked potentiation of their gastrointestinal effects. 5 At these doses antagonism of the hypotensive action of prostaglandin F2 by DPP was seldom seen but the gastrointestinal effect of prostaglandin F2Q was sometimes antagonized. 6 After treatment with DPP 100 ,ug kg-' minm1, high doses of prostaglandin were sometimes lethal.

“…Thus the mechanism by which its catalytic activity is controlled is clearly of interest. One possibility is that the synthesis of PGDH is controlled by blood concentrations of steroid or other hormones (Bedwani & Marley, 1975).…”

Section: Effect Of Cycloheximide On Pgdh In the Lungmentioning

confidence: 99%

Rapid Reduction of Prostaglandin 15‐hydroxy Dehydrogenase Activity in Rat Tissues After Treatment With Protein Synthesis Inhibitors

Blackwell

Flower

Vane

1975

1The capacity of rat kidneys to metabolize prostaglandins is rapidly lost when de novo protein synthesis is reduced by cycloheximide and puromycin. Enzyme activity declines to about half control values 45-75 min after a single dose of cycloheximide. Prostaglandin metabolism by the lung is also diminished. 2 These inhibitors apparently act by preventing the synthesis of new prostaglandin 15-hydroxy dehydrogenase enzyme. 3 The RNA synthesis inhibitor actinomycin D has no effect on metabolism. 4 It is concluded that prostaglandin dehydrogenase is a short-lived enzyme in the cell whose replacement depends upon de novo protein (but not RNA) synthesis. The implications of this finding are discussed.