metabolize

Nifursol 是一种具有口服活性的兽用抗生素，用于预防组织口炎。它快速代谢形成代谢标记物 3,5-二硝基水杨酸环肼，并能持续很长时间。它可研究沙门氏菌感染的家禽、家禽和水生动物的大肠杆菌肠胃病。

L-(-)-α-Methyldopa (MK-351) 是一种前药，在中枢神经系统中被代谢成 α-Methylepinephrine。它是 α-肾上腺素能激动剂，对 α2- adrenergic receptors 有选择性。

Flavone (2-Phenyl-4-chromone) 是内源性代谢产物的一种。

N-Acetyl-L-phenylalanine (N-Ac-Phenylalanine) 是一种大肠杆菌中的主要酰基氨基酸，由 L-苯丙氨酸和乙酰辅酶 A 合成。

Hexazinone 是一种三嗪家族的非选择性除草剂。它能够同光系统 II 电子传递链的 D-1 醌蛋白结合，抑制光合作用的发生。

(±)13-HODE cholesteryl ester was originally extracted from atherosclerotic lesions and shown to be produced by Cu2+-catalyzed oxidation of LDL. Later studies determined that 15-LO from rabbit reticulocytes and human monocytes were able to metabolize cholesteryl linoleate, a major component of LDL, to 13-HODE cholesteryl ester.

(±)9-HODE cholesteryl ester was originally extracted from atherosclerotic lesions and shown to be produced by Cu2+-catalyzed oxidation of LDL. Later studies determined that 15-LO from rabbit reticulocytes and human monocytes were able to metabolize cholesteryl linoleate, a major component of LDL, to 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. 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, whereas 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 the formation of leukotrienes may provide a basis for 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.