metabolize

Nifursol is a livestock feed additive and antiobiotic used to prevent the growth of histomonas.

N-Acetyl-L-phenylalanine (N-Ac-Phenylalanine) is an essential amino acid produced for medical, feed, and nutritional applications. It appears in large amount in urine of patients with phenylketonuria which is a human genetic disorder due to the lack of phenylalanine hydroxylase, the enzyme necessary to metabolize phenylalanine to tyrosine. Acetylphenylalanine is a product of enzyme phenylalanine N-acetyltransferase in the pathway phenylalanine metabolism.

Hexaflumuron is a chitin synthesis inhibitor used to bait and eliminate termite colonies. Termites are unable to metabolize hexaflumuron and clearance is slow, resulting in up to 100% elimination. Hexaflumuron has also been tested for use with the raisin

Flavone (2-Phenyl-4-chromone) have effects on CYP (P450) activity which are enzymes that metabolize most drugs in the body.

(±)13-HODE cholesteryl ester, initially extracted from atherosclerotic lesions, is produced via Cu2+-catalyzed oxidation of LDL. Subsequent studies revealed that 15-LO from rabbit reticulocytes and human monocytes could metabolize cholesteryl linoleate (a major LDL component) to 13-HODE cholesteryl ester.

(±)9-HODE cholesteryl ester, initially extracted from atherosclerotic lesions, is formed through Cu2+-catalyzed oxidation of LDL. Subsequent research demonstrated that 15-LO from rabbit reticulocytes and human monocytes can metabolize cholesteryl linoleate, a major LDL component, into 9-HODE cholesteryl ester.

(±)13-HDHA is an autoxidation product of docosahexaenoic acid (DHA) in vitro. It is also produced from incubations of DHA in rat liver, brain, and intestinal microsomes. Fresh water hydra was shown to metabolize DHA to 13(R)-HDHA, presumably via the 11R-lipoxygenase activity. (±)13-HDHA is a potential marker of oxidative stress in brain and retina where DHA is an abundant polyunsaturated fatty acid.

12(S)-HETE is a product of arachidonic acid metabolism through the 12-lipoxygenase pathway. It is primarily found in platelets, leukocytes, and to a lesser extent in smooth muscle cells. It enhances tumor cell adhesion to endothelial cells, fibronectin, and the subendothelial matrix. tetranor-12(S)-HETE is the major β-oxidation product resulting from peroxisomal metabolism of 12(S)-HETE in numerous tissues, and Lewis lung carcinoma cells. No biological function has yet been determined for tetranor-12(S)-HETE. Some data indicate it may play a role in controlling the inflammatory response in injured corneas. In some diseases (e.g., Zellweger's Syndrome) peroxisomal abnormalities result in the inability of cells to metabolize 12(S)-HETE, which may be responsible for symptoms of the disease. The tetranor derivative of 12(S)-HETE is available as a research tool for the elucidation of the metabolic fate of its parent compound.

20-hydroxy Prostaglandin F2α (20-hydroxy PGF2α) is the ω-oxidation product of PGF2α. Cultured type II alveolar cells from pregnant rabbits metabolize exogenous PGF2α via microsomal cytochrome P450 ω-oxidation, producing 20-hydroxy PGF2α and its 15-hydroxy PGDH metabolites [20-hydroxy PGF2α and 15-hydroxy PGDH]. Cells from male rabbits exhibit only the 15-hydroxy PGDH pathway.

12(S)-HEPE is a monohydroxy fatty acid synthesized from EPA by the action of 12-LO. Unstimulated neutrophils metabolize 12(S)-HEPE to 12(S),20-diHEPE, while stimulated neutrophils produce 5(S),12(S)-HEPE via the 5-lipoxygenase pathway. The competitive action of 12(S)-HEPE with arachidonic acid as a substrate for 5-LO in leukotriene formation may underlie the anti-inflammatory potential of ω-3 fatty acids.

11β-13,14-Dihydro-15-keto PGF2α, a PGD2 metabolite in the 15-hydroxy PGDH pathway, is formed in human males upon infusion or inhalation of tritiated PGD2, with peak plasma levels of both 11β-PGF2α and 11β-13,14-dihydro-15-keto PGF2α observed within 10 minutes. In human lung homogenates, PGD2 is metabolized firstly to 11β-PGF2α and subsequently to 11β-15-keto-PGF2α in the presence of NAD+, but not to 11β-13,14-dihydro-15-keto PGF2α. Conversely, guinea pig liver and kidney homogenates can metabolize PGD2 to 11β-13,14-dihydro-15-keto PGF2α via 11β-PGF2α, with both NAD+ and NADP+ being requisite for this conversion.