PGI2, 126.96.36.199, 188.8.131.52, 184.108.40.206, DHRS4, 220.127.116.11, 18.104.22.168, HPGD, 22.214.171.124, COX-2 (PTGS2), None, 12-13,14-Dihydro-PGJ2 delta, 126.96.36.199, PGH2, 188.8.131.52, 15-Hydroperoxyprostacyclin, 184.108.40.206, Arachidonic acid, 220.127.116.11, ALOX12B, 15-hydroperoxy-PGE1, PRDX5, 18.104.22.168, 13,14-dihydro-PGF2alpha, THAS, 22.214.171.124, 15-oxo-Prostaglandin H2, None, 6-Keto-prostaglandin E1, PGHD, 126.96.36.199, CYP4F12, 188.8.131.52, 5.3.3.-, ALDX, 184.108.40.206, 220.127.116.11, None, 15-oxo-Prostaglandin I2, 18.104.22.168, spontaneous, 22.214.171.124, 126.96.36.199, PRDX4, 188.8.131.52, None, 184.108.40.206, PTGIS, Prostaglandin B2, 220.127.116.11, 18.104.22.168, PGG2, 20-Hydroxy-prostaglandin H1, 22.214.171.124, 126.96.36.199, 15-Keto-PGF2alpha, 188.8.131.52, 12-hydroxyheptadeca-5,8,10-trienoic acid, 184.108.40.206, Prostaglandin J2, Prostaglandin F2 alpha, COX-1 (PTGS1), 220.127.116.11, 18.104.22.168, Thromboxane A2 , PGE2 , 1.13.11.-, 22.214.171.124, None, 126.96.36.199, PRDX1, 15-Hydroperoxy-PGE2, CBR2, PGD2, 13,14-Dihydro-15-keto-PGF2alpha, 188.8.131.52, Thromboxane B2 , Prostaglandin C2, AKR1C3, 5,6-Dihydro-15-keto-prostaglandin E2, LTB4DH, Prostaglandin A2, 13,14-dihydro-15-keto-PGE2, 15-hydroperoxy-5,8,10-heptadecatrienoic acid, 184.108.40.206, LOXE3, PGES, PRDX3, None, 6-Keto-prostaglandin F1alpha, Carbonyl reductase [NADPH] 3, PRDX2, CBR1, 15-keto-prostaglandin E2, 220.127.116.11, PGES2, 15-Hydroperoxy-PGD2, 11-epi-PGF2alpha, 9-Oxo-PGF2alpha, 15-Hydroperoxythromboxane B2, 18.104.22.168, PGDS
Prostaglandin 2 biosynthesis and metabolism FM
Prostaglandin biosynthesis starts with arachidonic acid that is oxidized to Prostaglandin H2 ( PGH2 ) by Prostaglandin G/H synthase 1 precursor ( COX-1 (PTGS1) ) or by Prostaglandin G/H synthase 2 precursor ( COX-2 (PTGS2) ) , , , , . An alternative reaction involves oxidation of arachidonic acid resulting in formation of Prostaglandin G2 ( PGG2 ) catalyzed either by COX-1 (PTGS1) ,  and COX-2 (PTGS2) , , or by Epidermis-type lipoxygenase 3 ( LOXE3 ) ,  and Arachidonate 12-lipoxygenase, 12R type ( ALOX12B ) , . COX-1 (PTGS1) and COX-2 (PTGS2) , ,  can oxidize PGH2 directly to PGG2, whereas PGG2 can be reduced directly to PGH2 by a number of enzymes, e.g., Peroxiredoxin-1 ( PRDX1 ), Peroxiredoxin-2 ( PRDX2 ), Thioredoxin-dependent peroxide reductase, mitochondrial precursor ( PRDX3 ), Peroxiredoxin-4 ( PRDX4 ) , Peroxiredoxin-5, mitochondrial precursor ( PRDX5 ) ,  ). This reduction is coupled with the oxidation of reduced glutathione.
PGH2 can be directly transformed to Prostaglandin E2 ( PGE2 ) by the Prostaglandin E synthase ( PGES ) ,  and Prostaglandin E synthase 2 ( PGES2 ) , , , and to Prostaglandin D2 ( PGD2 ) by the Alcohol dehydrogenase [NADP+] ( ALDX ) . PGD2 can also be formed by Aldo-keto reductase family 1 member C3 ( AKR1C3 ) with 11-epi-PGF2alpha as a precursor , .
There are various ways to form Prostaglandin F2 alpha ( PGF2 alpha ). One way is by reduction of the PGE2 catalyzed by Carbonyl reductase [NADPH] 1 ( CBR1 ) , , Carbonyl reductase [NADPH] 2 ( CBR2 ) , , Carbonyl reductase [NADPH] 3  and Dehydrogenase/reductase SDR family member 4 ( DHRS4 ) , . PGF2 alpha can also be synthesized from PGD2 in the reaction catalyzed by ALDX and AKR1C3 , . Another way involves transformation of PGH2 also catalyzed by AKR1C3 . PGE2 can also be reduced to 15-oxo-PGE2 either by 15-hydroxyprostaglandin dehydrogenase [NAD+] ( HPGD ) ,  or CBR1. The latter subsequently catalyzes the reduction of 15-oxo-PGE2 to 15-ketoprostaglandin F2 alpha ( 15-Keto-PGF2alpha ) that is in turn reduced by CBR1 to PGF2 alpha.
PGE2 loses water moiety and transforms to Prostaglandin A2 ( PGA2 ). The latter is further transformed to Prostaglandin C2 ( PGC2 ). PGC2 can be also transformed to Prostaglandin B2 ( PGB2 ) . PGD2 can be transformed to Prostaglandin J2 ( PGJ2 ). Prostaglandin I2 (prostacyclin) synthase ( PTGIS ) catalyzes dehydration on PGH2 resulting in the formation of Prostaglandin I2 ( PGI2 ) .
PGH2 is metabolized by a set of enzymes. Thromboxane A synthase 1 (platelet) ( THAS ) forms 12-hydroxyheptadeca-5,8,10-trienoic acid and malonic dialdehyde as a byproduct, Thromboxane A(,2 ) ,  and Thromboxane B2. Thromboxane A2 in its turn can spontaneously convert to Thromboxane B2. Prostaglandin E synthase ( PGES) and Prostaglandin E synthase 2 ( PGES2) catalyze the transformation of PGH2 to 15-hydroperoxy-PGE1 , , . Cytochrome P450, family 4, subfamily F, polypeptide ( CYP4F12 ) reduces PGH2 to 20-hydroxy-prostaglandin H1 , . This enzyme also catalyzes the reduction of PGE2 to 9-oxo-PGF2alpha. PGE2 can be transformed to 5,6-dihydro-15-keto-prostaglandin E2 by HPGD , .
PGE2 metabolite 15-oxo-PGE2 is reduced to 13,14-dihydro-15-keto-PGE2 by Prostaglandin reductase 1 ( LTB4DH ), while another metabolite 15-keto-PGF2alpha is also reduced by the same enzyme to 13,14-dihydro-15-keto-PGF2alpha. The latter product is subsequently transformed by CBR1 to 13,14-dihydro-PGF2alpha. 15-Keto-PGF2 alpha can also be formed from PGF2 alpha via the reaction catalyzed by CBR1  or HPGD , .
PGJ2 is metabolically transformed to 12-13,14-dihydro-PGJ2 delta.
THAS catalyzes the transformation of PGG2 to 15-hydroperoxy-5,8,10-heptadecatrienoic acid with Malonic dialdehyde as a byproduct, or to 15-hydroperoxythromboxane B2. PGES and PGES2 transform PGG2 to 15-hydroperoxy-PGE2 , . Prostaglandin D2 synthase (brain) ( PGHD ) and Prostaglandin D2 synthase 2 hematopoietic ( PGDS ) can also catalyze formation of 15-hydroperoxy-PGD2 , , . PTGIS hydroxylates PGG2 to 15-hydroperoxyprostacyclin.
PGI2 also undergoes significant metabolic transformation. It can be hydrolyzed to form 6-keto-prostaglandin F1alpha that is subsequently oxidized to 6-keto-prostaglandin E1 . Another pathway involves PGI2 oxidation to 15-oxo-prostaglandin I2  that is finally transformed by PTGIS to 15-oxo-prostaglandin H2.