| Name | cytochrome P450 (protein family or complex) |
|---|---|
| Synonyms | cytochrome P450; cytochrome P 450; CYP450; CYP 450 |
| Name | diphenylamine |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 2592379 | Jain SK: Hyperglycemia can cause membrane lipid peroxidation and osmotic fragility in human red blood cells. J Biol Chem. 1989 Dec 15;264(35):21340-5. -induced membrane lipid peroxidation and osmotic fragility were blocked when RBC were pretreated with an inhibitor of metabolism; with an antioxidant; with para-chloromercurobenzoate and inhibitors of the cytochrome P-450 system; or with dimethylfurane, diphenylamine, and thiourea, scavengers of radicals. |
31(0,1,1,1) | Details |
| 1259955 | Wang HP, Kimura T: Ferrous ion-mediated cytochrome P-450 degradation and lipid peroxidation in adrenal cortex mitochondria. Biochim Biophys Acta. 1976 Mar 12;423(3):374-81. Yet, diphenylamine proved to be a powerful inhibitor for both reactions, suggesting the involvement of a radical species. |
3(0,0,0,3) | Details |
| 6533036 | Appel KE, Ruhl CS, Hildebrandt AG: Metabolic inactivation of N-nitrosamines by cytochrome P-450 in vitro and in vivo. IARC Sci Publ. 1984;(57):443-51. Diphenylamine was also detected. |
3(0,0,0,3) | Details |
| 3679347 | Appel KE, Schoepke M, Scheper T, Gorsdorf S, Bauszus M, Ruhl CS, Kramer R, Ruf HH, Spiegelhalder B, Wiessler M, et al.: Some aspects of cytochrome P450-dependent denitrosation of N-nitrosamines. IARC Sci Publ. 1987;(84):117-23. One metabolite was identified as diphenylamine; others were suspected to be the 4-hydroxylated derivative and its corresponding quinoneimine. |
2(0,0,0,2) | Details |
| 3031080 | Appel KE, Gorsdorf S, Scheper T, Ruf HH, Ruhl CS, Hildebrandt AG: Metabolic denitrosation of diphenylnitrosamine: a possible bioactivation pathway. J Cancer Res Clin Oncol. 1987;113(2):131-6. In view of the metabolic capacity of hepatocytes and the chemical structure of nitrosodiphenylamine it seems likely that cytochrome P-450-dependent, reductive denitrosation might be necessary for exerting this effect. One metabolite was identified as diphenylamine whereas the others were identified as a ring-hydroxylated derivative of diphenylamine and its corresponding quinoneimine. |
1(0,0,0,1) | Details |
| 8268299 | Semak IV, Pikulev AT: [The functional status of the xenobiotic biotransformation system in poisoning animals with diphenylamine and N-nitrosodiphenylamine]. Biokhimiia. 1993 Oct;58(10):1562-5. There was an increase in the total content of cytochrome P-450 and the activity of -cytochrome P-450 reductase as well as a marked elevation of activity of microsomal glutathione S-transferase. |
1(0,0,0,1) | Details |
| 8769983 | Amlal H, Legoff C, Vernimmen C, Paillard M, Bichara M: Na (+)-K+(NH4+)-2Cl- cotransport in medullary thick ascending limb: control by PKA, PKC, and 20-HETE. Am J Physiol. 1996 Aug;271(2 Pt 1):C455-63. Cell pH was monitored in suspensions of medullary thick ascending limbs (MTALs) of rat kidney to determine possible effects of various transduction pathways on apical Na (+)-K+ (NH4+)-2Cl- cotransport, the activity of which was measured as the bumetanide-sensitive component of cell acidification caused by abrupt exposure to 4 mM NH4Cl. 8-Bromoadenosine 3',5'-cyclic monophosphate stimulated cotransport activity through activation of 3',5'-cyclic monophosphate (cAMP)-dependent protein kinase (PKA), since the cAMP effect was abolished by N-[2-(p- bromocinnamylamino) ethyl]-5-isoquinolinesulfonamide (H-89); stimulation by cAMP (P < 0.02) was observed even when other Na+, Cl-, and K+ carriers were blocked by ouabain, diphenylamine-2-carboxylate, and barium, which indicates that cotransport was directly affected by PKA. Inhibition by or ionomycin was abolished by econazole and SKF-525A that inhibit cytochrome P-450-dependent monoxygenase, which produces 20-HETE from in the MTAL, and the ionomycin effect was prevented when phospholipase A2 (PLA2) was blocked by 4-bromophenacyl or oleyloxyethyl |
1(0,0,0,1) | Details |
| 19429231 | Li Y, Qi XM, Xue X, Wu XF, Wu YF, Chen M, Xing GZ, Luan Y, Ren J: The relationship between diphenylamine structure and NSAIDs-induced hepatocytes injury. Toxicol Lett. 2009 Apr 25;186(2):111-4. Epub 2009 Jan 16. |
0(0,0,0,0) | Details |
| 3619641 | Appel KE, Gorsdorf S, Scheper T, Bauszus M, Hildebrandt AG: Enzymatic denitrosation of diphenylnitrosamine: activation or inactivation?. Arch Toxicol. 1987;60(1-3):204-8. In view of the metabolic capacity of hepatocytes and the chemical structure of nitrosodiphenylamine, it seems likely that cytochrome P-450-dependent, reductive denitrosation might be necessary for exerting this effect. One metabolite was identified as diphenylamine, whereas the others were characterized as p-hydroxydiphenylamine and its corresponding quinoneimine. |
1(0,0,0,1) | Details |
| 7141576 | Wakabayashi K, Nagao M, Kawachi T, Sugimura T: Mechanism of appearance of mutagenicity of N-nitrosodiphenylamine with norharman. IARC Sci Publ. 1982;(41):695-707. N,N-Diphenylamine (DPhA), a denitrosated derivative of NDPhA, was also mutagenic to S. typhimurium TA98 when norharman was present. The denitrosation eyzme activity of NDPhA was mainly recovered in the microsomal fraction, and the enzyme seemed to be a cytochrome P-450 monooxygenase system. |
1(0,0,0,1) | Details |