Prostaglandin Dehydrogenase

Marrazzi, Mary Ann; Andersen, N H

doi:10.1007/978-1-4613-4544-2_4

Cited by 11 publications

(6 citation statements)

References 29 publications

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“…One possible explanation for the result could be the destruction of prostaglandin dehydrogenase by the oxidant gas. This hypothesis is consistent with the observed susceptibility to inactivation of prostaglandin dehydrogenase during purification (Marrazzi & Anderson, 1974).…”

Section: _______________0supporting

confidence: 91%

Inhibition of pulmonary prostaglandin metabolism by exposure of animals to oxygen or nitrogen dioxide

Chaudhari¹,

Sivarajah²,

Warnock³

et al. 1979

Biochemical Journal

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The effects of exposure of animals to 100% O2 and NO2 on the rate of prostaglandin metabolism by lung and kidney were studied in vitro. Exposure of guinea pigs to 100% O2 for 48 h inhibited the metabolism of prostaglandin F2 alpha by both NAD+- and NADP+-dependent prostaglandin dehydrogenase in lung, but had no effect on the metabolism in kidney. Succinate dehydrogenase, but not glucose 6-phosphate dehydrogenase, in guinea-pig lung was inhibited by exposure to 100% O2. Exposure to 46 p.p.m. but not 16 or 29 p.p.m. NO2 for 6 h inhibited guinea-pig lung prostaglandin dehydrogenase in vitro. The inhibition of pulmonary prostaglandin dehydrogenase by exposure to 100% O2 or to 49 p.p.m. NO2 was dependent on the duration of exposure, but returned to control values within 7 days after cessation of the exposure. The pulmonary transport system responsible for removing circulating prostaglandins from the blood was not affected by exposure to 100% O2 as measured by using the isolated perfused lung. Kinetic analysis of the inhibition of pulmonary prostaglandin dehydrogenase activity in guinea pig exposed to 100% O2 showed non-competitive inhibition with respect to both prostaglandin F2 alpha and NAD+, which suggests destruction or inactivation of the enzyme. Pulmonary prostaglandin dehydrogenase appears to be inhibited by exposure to oxidant gases, which may lead to elevated prostaglandin concentrations in the lungs or in the systemic circulation.

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Section: _______________0supporting

confidence: 91%

Inhibition of pulmonary prostaglandin metabolism by exposure of animals to oxygen or nitrogen dioxide

Chaudhari¹,

Sivarajah²,

Warnock³

et al. 1979

Biochemical Journal

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“…First, the secondary alcohol group at C-15 is oxidized by 15-hydroxyprostanoate dehydrogenase. 76,77 In the second step, the reduction of D 13 -double bond is catalyzed by D 13 -reductase. The half-life of 15-keto-dihydro-PGF 2a is less than about 8 min in the circulation.…”

Section: Metabolism Of Pgf 2amentioning

confidence: 99%

Novel cyclooxygenase‐catalyzed bioactive prostaglandin F_2α from physiology to new principles in inflammation

Basu

2006

Medicinal Research Reviews

109

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Prostaglandin F2alpha (PGF2alpha), a foremost stable vasoactive cyclooxygenase (COX)-catalyzed prostaglandin, regulates a number of key physiological functions such as luteolysis, ovarian function, luteal maintenance of pregnancy, and parturition as a constitutive part of ongoing reproductive processes of the body. It has recently been implicated in the regulation of intricate pathophysiological processes, such as acute and chronic inflammation, cardiovascular and rheumatic diseases. Since the discovery of a second isoform of COXs, it has been shown that PGF2alpha can be formed in vivo from arachidonic acid through both isoforms of COXs, namely cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2). Being synthesized in various parts of the body, it metabolizes instantly to a number of rather inactive metabolites mainly in the lungs, liver, kidney, and efficiently excretes into the urine. 15-Keto-dihydro-PGF2alpha, a major stable metabolite of PGF2alpha that reflects in vivo PGF2alpha biosynthesis, is found in larger quantities than its parent compound in the circulation and urine in basal physiological conditions, with short-lived pulses during luteolysis, induced termination of pregnancy and parturition, and is increased in tissues and various body fluids during acute, sub-chronic, and severe chronic inflammation. Further, the close relationship of PGF2alpha with a number of risk factors for atherosclerosis indicates its major role in inflammation pathology. This review addresses multiple aspects of PGF2alpha in addition to its emerging role in physiology to inflammation.

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“…Indomethacin has been shown to affect calcium movement into tissue [19], to inhibit phosphodiesterase activity in vitro [6], and also to affect the activity of catabolic enzymes, the prostaglandin dehydrogenases [17]. Although these actions have been attributed to indomethacin, it is not possible at this time to state the predominant effect of the drug at a specific dose.…”

Section: Discussionmentioning

confidence: 99%

Angiotensin Analogs: Effect of Prostaglandin Synthesis Inhibitor

Hall¹,

Gurchinoff²,

Khosla³

et al. 1978

J Vasc Res

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Structurally different inhibitors of prostaglandin synthesis reversed the antagonistic activity of the angiotensin II analog 1-sarcosine, 8-threonine angiotensin II. In isolated rabbit aorta, indomethacin or ETYA (eicosa 5, 8, 11, 14, tetraynoic) reversed the antagonism of the angiotensin II analog without affecting the dose response curves to angiotensin II. Both indomethacin and ETYA were able to reverse the tachyphylaxis to angiotensin II. Investigating the possibility that indomethacin could affect the binding of angiotensin II, it was found that at doses of indomethacin higher than 10^–5 m, binding of tritiated angiotensin to isolated adrenal cortical cells was reduced. It is postulated that indomethacin may have more than one effect on angiotensin, possessing a concentration-dependent effect on binding and prostaglandin synthesis.

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Prostaglandin Dehydrogenase

Cited by 11 publications

References 29 publications

Inhibition of pulmonary prostaglandin metabolism by exposure of animals to oxygen or nitrogen dioxide

Inhibition of pulmonary prostaglandin metabolism by exposure of animals to oxygen or nitrogen dioxide

Novel cyclooxygenase‐catalyzed bioactive prostaglandin F_2α from physiology to new principles in inflammation

Angiotensin Analogs: Effect of Prostaglandin Synthesis Inhibitor

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Prostaglandin Dehydrogenase

Cited by 11 publications

References 29 publications

Inhibition of pulmonary prostaglandin metabolism by exposure of animals to oxygen or nitrogen dioxide

Inhibition of pulmonary prostaglandin metabolism by exposure of animals to oxygen or nitrogen dioxide

Novel cyclooxygenase‐catalyzed bioactive prostaglandin F2α from physiology to new principles in inflammation

Angiotensin Analogs: Effect of Prostaglandin Synthesis Inhibitor

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Resources

About

Novel cyclooxygenase‐catalyzed bioactive prostaglandin F_2α from physiology to new principles in inflammation