Disease relevance of Cyp2c23

• Tumor necrosis factor alpha blockade increases renal Cyp2c23 expression and slows the progression of renal damage in salt-sensitive hypertension [1].

High impact information on Cyp2c23

• The kidney cytochrome P-450 2C23 arachidonic acid epoxygenase is upregulated during dietary salt loading [2].
• A cDNA containing an open reading frame coding for the rat kidney cytochrome P-450 arachidonic acid epoxygenase was isolated from a male rat kidney cDNA library [3].
• These results established that the chirality of the hepatic arachidonic acid epoxygenase is under regulatory control and confirm cytochromes P-450 IIB1 and IIB2 as two of the endogenous epoxygenases induced in vivo by phenobarbital [4].
• Role of P-450 arachidonic acid epoxygenase in the response of cerebral blood flow to glutamate in rats [5].
• Molecular characterization of an arachidonic acid epoxygenase in rat brain astrocytes [6].

Chemical compound and disease context of Cyp2c23

• These data suggest that TNF-alpha contributes to downregulation of Cyp2c23, blood pressure regulation, and renal injury in angiotensin high-salt hypertension [1].

Biological context of Cyp2c23

• Epoxyeicosatrienoic acids (EETs) and dihydroxyeicosatrienoic acids, products of the cytochrome P450 arachidonic acid epoxygenase pathway, have been shown to affect electrolyte transport in the kidney; however, the effects of these compounds on airway epithelial ion transport have not been investigated [7].
• The imidazole derivatives, ketoconazole and clotrimazole, are potent and selective inhibitors of the arachidonic acid epoxygenase and lipoxidase-like activities of phenobarbital-induced rat liver microsomal fractions (IC50, 2.0 and 0.3 microM, respectively) [8].

Anatomical context of Cyp2c23

• By a combination of chromatographic and mass spectrometric techniques, we have identified epoxyeicosatrienoic acids as reaction products and thus documented the presence of an NADPH-dependent arachidonic acid epoxygenase activity in rat adenohypophysis [9].
• Epoxyeicosatrienoic acids, products of the cytochrome P-450-NADPH dependent arachidonic acid epoxygenase activity, are potent and selective mediators for the in vitro release of either insulin or glucagon from preparations of isolated rat pancreatic islets [10].

Associations of Cyp2c23 with chemical compounds

• Renal expression of Cyp2c23 decreased, whereas renal epoxide hydrolase expression increased in angiotensin high-salt rats [1].
• On the basis of mRNA abundance and the close similarities between the regio- and stereochemical selectivity of the recombinant and kidney microsomal proteins, we concluded that cytochrome P-450 2C23 is the predominant enzyme isoform responsible for arachidonic acid epoxidation in the rat kidney [3].
• The arachidonic acid epoxygenase metabolite 14,15-epoxyeicosatrienoic acid is further metabolized by rat liver microsomal fractions to regioisomeric diepoxides and epoxyalcohols [11].

Regulatory relationships of Cyp2c23

• Growth hormone secretion was stimulated in vitro by products of arachidonic acid epoxygenase, the epoxyeicosatrienoic acids [12].

Other interactions of Cyp2c23

• Etanercept treatment increased Cyp2c23 expression and lowered epoxide hydrolase expression [1].
• In contrast, pretreatment of somatotrophs with an 11,12-isonitrile analogue of arachidonic acid that inhibits arachidonic acid epoxygenase, resulted in a 20-25% inhibition of growth hormone-releasing hormone-stimulated growth hormone release [12].

Analytical, diagnostic and therapeutic context of Cyp2c23

• Molecular cloning, expression, and enzymatic characterization of the rat kidney cytochrome P-450 arachidonic acid epoxygenase [3].
• Inhibition and immunoelectrophoresis experiments using antibodies raised against recombinant P-450s 2C11 and 2C23 demonstrated that P-450 2C23 is the major 2C arachidonic acid epoxygenase in the rat kidney and the renal P-450 isoform regulated by excess dietary salt intake [2].
• We tested the hypothesis that experimental TIA induces expression of P450 2C11, an arachidonic acid epoxygenase that produces vasodilator epoxyeicosatrienoic acids, leading to increased tissue perfusion and reduced stroke damage [13].

References