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2350-01-8

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  • CAS Number:
  • 2350-01-8
  • Name:
  • 1,4-Benzenediamine,N1,N1-diphenyl-

  • Superlist Name:
  • N,N-Diphenyl-p-phenylenediamine
  • Molecular Structure:
  • Formula:
  • C18H16N2
  • Molecular Weight:
  • 260.34
  • Synonyms:
  • 1,4-Benzenediamine,N,N-diphenyl- (9CI);p-Phenylenediamine, N,N-diphenyl- (7CI,8CI);4-(Diphenylamino)aniline;4-(N,N-Diphenylamino)aniline;4-Aminotriphenylamine;N,N-Diphenyl-1,4-phenylenediamine;N,N-Diphenyl-4-aminoaniline;N-(4-Aminophenyl)-N,N-diphenylamine;NSC231610;p-(Diphenylamino)aniline;p-Aminotriphenylamine;N,N-diphenylbenzene-1,4-diamine;
  • Density:
  • 1.168 g/cm3
  • Boiling Point:
  • 436.9 °C at 760 mmHg
  • Flash Point:
  • 193.3 °C

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CAS No.2350-01-8 N,N-Diphenyl-p-phenylenediamineCompetitive Product

DetailDesc:1.Name:N-p-aminophenyl-diphenylamine 2.CAS#:2350-01-8 3.Molecular formula:C18H16N2 4.Molecular weight:260.34

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CAS No.2350-01-8 N,N-Diphenyl-p-phenylenediamine

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Reference

Protection with butylated hydroxytoluene and other compounds against intoxication and mortality caused by hexachlorophene
Protection with butylated hydroxytoluene and other compounds against intoxication and mortality caused by hexachlorophene. Hanig, J. P.; Yoder, P. D.; Krop, S. (Div. Drug Biol., Food and Drug Adm., Washington, DC 20204, USA). Food Chem. Toxicol., 22(3), 185-9 (English) 1984. CODEN: FCTOD7. ISSN: 0278-6915. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) The antioxidants BHT [128-37-0] and ethoxyquin [91-53-2] protected rats against intoxication and mortality normally produced by hexachlorophene (HCP)(I) [70-30-4] (100 mg/kg). BHT also prevented the elevation of cerebrospinal fluid pressure, a central nervous system effect of HCP poisoning. In addn., both phenobarbital [50-06-6] and SKF 525A [62-68-0] protected against HCP poisoning, with the barbiturate also offering significant protection against triethyltin [997-50-2]. L-Ascorbic acid [50-81-7], vitamin E [1406-18-4], N,N-diphenyl-p-phenylenediamine [2350-01-8], and glutathione [70-18-8] and oxidized glutathione [27025-41-8] over a range of doses were ineffective in preventing HCP lethality. The protective effect of phenobarbital against HCP and triethyltin intoxication further supports existing evidence of a common or similar mechanism of toxic action for these 2 structurally dissimilar compds.
Protective effects of antioxidants against benomyl-induced lipid peroxidation and glutathione depletion in rats
Protective effects of antioxidants against benomyl-induced lipid peroxidation and glutathione depletion in rats. Banks, Donna; Soliman, Magdi R. I. (College of Pharmacy and Pharmaceutical Sciences, Florida A and M University, Tallahassee, USA). Toxicology, 116(1-3), 177-181 (English) 1997 Elsevier. CODEN: TXCYAC. ISSN: 0300-483X. DOCUMENT TYPE: Journal CA Section: 4 (Toxicology) The present in vivo study was designed to examine the effects of the antioxidants, N,N-diphenyl-p-phenylenediamine (DPPD) and a 21-aminosteroid (U74389G), on Me 1-(butylcarbamoyl)-2-benzimidazole-carbamate (benomyl)-induced lipid peroxidn. and glutathione depletion in rats. Male Sprague-Dawley rats weighing 200-250 g were used in this study and were fasted for 8-12 h before treatment. Benomyl (200 mg/kg/day in olive oil) was administered orally for 7 days to groups of untreated rats and to rats pretreated with two doses (15 mg/kg) of either DPPD or U74389G. Benomyl treatment resulted in a significant increase in serum hydroperoxides and a significant decline in hepatic reduced glutathione (GSH) levels. These results indicate that benomyl induces lipid peroxidn. and glutathione depletion in rats. Benomyl-induced lipid peroxidn. was blocked by DPPD pretreatment but was not significantly altered by U74389G. However, both antioxidants, DPPD and U74389G, were able to inhibit glutathione depletion induced by benomyl. The present findings indicate that the in vivo toxicity of benomyl may be assocd. 2350-01-8 and 17804-35-2 are just another two chemicals used in this study. with oxidative stress to cellular membranes and that some degree of protection against this toxicity could be afforded by antioxidants. .
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