Disease relevance of PGDH

• PGDH activity in the placenta was significantly (p < 0.01) decreased in growth-restricted rats and remained low even after fetal weight recovered [1].

High impact information on PGDH

• However, the glycosides did not affect the enzymatic inactivation of radiolabelled prostaglandin F2 alpha by semi-purified bovine lung prostaglandin 15-hydroxydehydrogenase (PGDH) or in 100,000 g supernatants prepared from homogenised rat stomach [2].
• The results show that the capacity of flavonoids to enhance prostaglandin formation is associated with the presence of glycosidic substitution, whereas PGDH inhibition requires its absence [2].
• Three of the four aglycones (quercetin, kaempferol, isoscutellarein, in descending order of potency) were inhibitory to PGDH with ID50 values in the range 130-2100 microM [2].
• These results suggest that the inhibitory action of nafazatrom on 15-OH PGDH contributes to its antithrombotic effect by prolonging the biological half-life of PGI2 [3].
• As 15-OH PGDH, the key prostaglandin (PG) catabolizing enzyme, inactivates PGI2 as well as PGE2 and PGF2 alpha, inhibition of this enzyme can result in increased levels of PGI2 [3].

Biological context of PGDH

• The IC50 for inhibition of 15-OH PGDH was estimated to be 18.5 microM when [3H]PGF2 alpha was used as substrate [3].

Anatomical context of PGDH

• Initial studies demonstrated that chronic ethanol administration to male rats results in an impaired ability on the part of these animals to catabolize prostaglandins via renal prostaglandin dehydrogenase (PGDH) but no effect was observed on the synthesis of thromboxanes by blood platelets from these same animals [4].

Associations of PGDH with chemical compounds

• Nafazatrom also inhibited catabolism by 15-OH PGDH of [3H]PGI2-ME to [3H]6,15-diketo-PGF1 alpha ME [3].

References