Page last updated: 2024-10-24

prostaglandin catabolic process

Definition

Target type: biologicalprocess

The chemical reactions and pathways resulting in the breakdown of prostaglandin. [GO_REF:0000068, GOC:BHF, GOC:rl, GOC:TermGenie, PMID:25290914]

Prostaglandin catabolism is a crucial process in the regulation of prostaglandin levels in the body. Prostaglandins are lipid compounds derived from fatty acids that play a diverse range of physiological roles, including inflammation, pain, fever, and blood clotting. Their catabolism is essential for maintaining homeostasis and preventing excessive or prolonged prostaglandin activity.

The primary enzymes responsible for prostaglandin catabolism are prostaglandin dehydrogenases (PGDH) and 15-hydroxyprostaglandin dehydrogenase (15-PGDH). These enzymes act on the prostaglandin molecule, primarily targeting the 15-hydroxyl group, and oxidize it, leading to the formation of inactive metabolites.

PGDH is a NAD+-dependent enzyme that catalyzes the initial step in prostaglandin catabolism, converting prostaglandin E2 (PGE2) to 15-keto-PGE2. 15-PGDH is a cytosolic enzyme that further oxidizes 15-keto-PGE2 to 13,14-dihydro-15-keto-PGE2, ultimately leading to the formation of inactive metabolites that can be excreted in the urine.

Prostaglandin catabolism is tightly regulated by various factors, including hormones, cytokines, and drugs. For instance, certain hormones like estrogen and progesterone can stimulate PGDH activity, leading to decreased prostaglandin levels. Similarly, inflammatory cytokines like TNF-alpha can inhibit PGDH activity, resulting in elevated prostaglandin levels and increased inflammation.

Dysregulation of prostaglandin catabolism can contribute to several pathological conditions. For example, reduced PGDH activity is associated with increased prostaglandin levels and exacerbated inflammatory responses in conditions like rheumatoid arthritis and Crohn's disease. Conversely, increased PGDH activity can lead to reduced prostaglandin levels and potentially contribute to conditions like premenstrual syndrome and infertility.

In summary, prostaglandin catabolism is a complex and essential process that regulates prostaglandin levels in the body, playing a crucial role in inflammation, pain, and other physiological processes. Understanding the mechanisms of prostaglandin catabolism and its regulation is essential for developing effective therapies for a wide range of diseases and conditions.'
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Proteins (2)

ProteinDefinitionTaxonomy
Phosphatidylserine lipase ABHD16AA phosphatidylserine lipase ABHD16A that is encoded in the genome of human. [PRO:DNx, UniProtKB:O95870]Homo sapiens (human)
Acyl-protein thioesterase 2An acyl-protein thioesterase 2 that is encoded in the genome of human. [PRO:DNx, UniProtKB:O95372]Homo sapiens (human)

Compounds (7)

CompoundDefinitionClassesRoles
benzo(b)thiophene-2-boronic acidbenzo(b)thiophene-2-boronic acid: inhibits AmpC beta-lactamase; structure in first source
1,6-bis(cyclohexyloximinocarbonyl)hexane1,6-bis(cyclohexyloximinocarbonyl)hexane: selective inhibitor of canine platelet diglyceride lipasecarbamate ester;
organonitrogen compound
benzeneboronic acidboronic acids
1,1'-biphenyl-4-yl-boronic acid
orlistatorlistat : A carboxylic ester resulting from the formal condensation of the carboxy group of N-formyl-L-leucine with the hydroxy group of (3S,4S)-3-hexyl-4-[(2S)-2-hydroxytridecyl]oxetan-2-one. A pancreatic lipase inhibitor, it is used as an anti-obesity drug.

Orlistat: A lactone derivative of LEUCINE that acts as a pancreatic lipase inhibitor to limit the absorption of dietary fat; it is used in the management of obesity.
beta-lactone;
carboxylic ester;
formamides;
L-leucine derivative
anti-obesity agent;
bacterial metabolite;
EC 2.3.1.85 (fatty acid synthase) inhibitor;
EC 3.1.1.3 (triacylglycerol lipase) inhibitor
palmostatin bpalmostatin B: inhibits acyl protein thioesterase 1; structure in first source
palmostatin mpalmostatin M: inhibits acyl protein thioesterases 1 and 2; structure in first source