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At least 19 recordsLinked to original sources
PubMed2001

Spectroelectrochemical characterization of Si-bridged diphenylamines: influence of Si-bridging upon electronic structures of diphenylamines.

Spectroelectrochemical properties of monosilane bridged diphenylamine (5,10-dihydro-2,8-diphenyl-5, 10,10-trimethylphenazasiline, Phenaz) and disilane bridged diphenylamine (2,8-diphenyl-10,11-dihydro-10,11-disila-5,10,10,11,11-pentamethyldibenzo[b,f]azepine, DSiAzep) were investigated. The electrochemical oxidation of Phenaz was reversible and its cyclic voltammogram was almost the same shape as that of diphenylamine (DPA). The electrochemical oxidation of DSiAzep was followed by irreversible reactions leading to the cleavage of the Si-Si bond. On electrochemical oxidations of Phenaz and DPA, the formation of a stable radical cation was observed with UV-Vis spectroscopy. In comparison with the absorption characteristics of oxidized radical cations, it was seen that the oxidized radical cation of Phenaz was more delocalized than that of DPA. In the same way, absorption characteristics of oxidized DSiAzep were observed to be different from those observed in Phenaz and DPA.

Journal Article↗
PubMed2005

1-Methylcyclopropene interactions with diphenylamine on diphenylamine degradation, alpha-farnesene and conjugated trienol concentrations, and polyphenol oxidase and peroxidase activities in apple fruit.

1-Methylcyclopropene (1-MCP) is a new technology that is applied commercially to inhibit ethylene action in apple fruit, but its interactions with existing technologies such as diphenylamine (DPA) for control of superficial scald development in fruit during and after storage is unknown. To investigate possible interactions between 1-MCP and DPA, Delicious apples were untreated or treated with 2 g L(-1) DPA, and then with or without 1 microL L(-1) 1-MCP. Ethylene production and respiration rates of fruit were measured immediately following treatment, and fruit was stored at 0.5 degrees C for 12 weeks. Internal ethylene concentrations (IEC), alpha-farnesene and conjugated trienol (CTol) concentrations, activities of peroxidase and polyphenol oxidase (PPO), and DPA levels in the skin of the fruit were measured at intervals during storage. 1-MCP reduced the rate of DPA loss from peel tissue so that by 12 weeks of storage concentrations of the chemical were 25% higher than in untreated fruit. 1-MCP, with and without DPA, markedly inhibited ethylene production and respiration rates, maintained low IEC and alpha-farnesene and CTol concentrations, while DPA had little effect on these factors except inhibition of CTol accumulation. Treatment effects on peroxidase and PPO activities were inconsistent.

Catechol Oxidase↗
PubMed2005

Relationship of superficial scald development and alpha-farnesene oxidation to reactions of diphenylamine and diphenylamine derivatives in Cv. Granny Smith apple peel.

Cv. Granny Smith apple fruit, treated at harvest with aqueous emulsions containing diphenylamine (DPA) and DPA derivatives, were evaluated for the peel disorder superficial scald (scald) after 6 months of cold storage at 1 degrees C plus 0 or 7 days at 20 degrees C. Metabolism of these derivatives and alpha-farnesene oxidation were also evaluated after 6 months. Derivatives substituted at the para position prevented scald, but scald developed on fruit treated with derivatives substituted in the amino, ortho, or meta positions. The extent of scald control was also dependent on the chemical nature of the functional group used to derivatize DPA. Hydroxylation of DPA and DPA derivatives during storage was not associated with scald control. Methoxylated DPA derivatives produced during storage resulted from O-methylation of C-hydroxylated derivatives rather than C-methoxylation of DPA. N-Nitrosodiphenylamine provided partial scald control, possibly resulting from its degradation to DPA, indicating that the amino hydrogen of DPA may be crucial for scald control. Results suggest that functional group position and chemical properties both contribute to the efficacy of DPA derivatives for scald control.

Cold Temperature↗
PubMed2006

Influence of ethylene action, storage atmosphere, and storage duration on diphenylamine and diphenylamine derivative content of Granny Smith apple peel.

The application of diphenylamine (DPA) to prevent the apple peel disorder superficial scald can result in accumulation of a number of DPA derivatives resulting from C-nitration, C-hydroxylation, O-methylation, and N-nitrosation during fruit storage. As the presence of these compounds may be indicative of metabolic processes leading to superficial scald development, the contents of DPA and DPA derivatives were determined in fruits treated at harvest with DPA or DPA plus the ethylene action inhibitor 1-methylcyclopropene (1-MCP), which also prevents scald development. Influences of fruit maturity, storage environment, storage duration, and a 14 day poststorage ripening period on accumulation of DPA metabolites were also assessed. Poststorage ripening, 1-MCP treatment, and controlled atmosphere storage had varied effects on DPA derivative contents suggesting that reactive oxygen and nitrogen species, such as *OH, *NO, and *NO2, or enzyme-catalyzed reactions may be present during certain ripening and senescence-related physiological processes. Definitive correlations between superficial scald incidence and contents of specific derivatives were not observed.

Diphenylamine↗
PubMed1990

Diphenylamine-induced renal papillary necrosis and necrosis of the pars recta in laboratory rodents.

The nephrotoxicity of diphenylamine, the parent compound of the mefenamate family of nonsteroidal anti-inflammatory drugs, was evaluated in male Syrian hamsters, male Sprague-Dawley rats, and male Mongolian gerbils. Total renal papillary necrosis was observed in four of ten, seven of ten, and six of ten male Syrian hamsters orally treated with diphenylamine at respective doses of 400 mg/kg body weight/day, 600 mg/kg body weight/day, and 800 mg/kg body weight/day. Total renal papillary necrosis was also observed in five of ten and four of ten male Syrian hamsters intraperitoneally treated with diphenylamine at respective doses of 600 mg/kg body weight/day and 800 mg/kg body weight/day. Focal intermediate renal papillary necrosis was induced in two hamsters orally given diphenylamine at 600 mg/kg body weight/day and in two of ten hamsters intraperitoneally given diphenylamine at 800 mg/kg body weight/day. Apex-limited necrosis of the medullary interstitial cells and vasa recta and degeneration of the renal interstitial matrix occurred in two Sprague-Dawley rats orally administered diphenylamine at 800 mg/kg body weight/day. Degeneration and necrosis of the pars recta was induced in seven of ten hamsters intraperitoneally given diphenylamine at 400 mg/kg body weight/day. Gross and microscopic renal lesions were not observed in any Mongolian gerbils. It was concluded that the Syrian hamster is more susceptible to the papillotoxic effects of diphenylamine than the Sprague-Dawley rat and the Mongolian gerbil. Renal papillary necrosis in the Syrian hamster treated orally with diphenylamine is reproducible, is of short onset, and is induced in a high proportion of the hamsters (70-90%).(ABSTRACT TRUNCATED AT 250 WORDS)

Aniline Compounds↗
PubMed1976

Comparison of human polycystic and medullary cystic kidney disease with diphenylamine-induced cystic disease.

Because of difficulty in obtaining cystic human kidneys for functional and morphologic study, animal models are receiving increasing attention. Most prominent among them is the renal cystic disease that is induced in rats through feeding of the antioxidant, diphenylamine, The present study examined the morphology of adult polycystic and medullary cystic kidney disease in man using scanning electron microscopy and compared them with diphenylamine-induced cystic kidney disease in rats. Diphenylamine nephropathy was induced by feeding rats 1 per cent diphenylamine for 12 to 18 months. All types of cystic disease showed changes in the renal corpuscles, including dilation of Bowman's space, podocyte fusion and degeneration, and basement membrane thickening. Cysts were noted along the entire nephron in polycystic and diphenylamine-induced cystic disease but only along the collecting ducts in medullary cystic disease. Cysts in polycystic disease were large and lined by flattened epithelium. Collecting duct cysts in diphenylamine cystic disease were lined by cells of irregular size and shape suggestive of cell hypertrophy and/or hyperplasia, whereas cysts of medullary cystic disease were lined by flattened epithelium except where the nephron entered or left the cyst. Cast material was generally found in the cysts of diphenylamine-induced and polycystic kidney disease but not medullary cystic disease. Atrophic glomeruli and tubules were found in all three diseases. Complete tubular obstruction was found in none; however, larger cysts frequently impinged on adjacent tubules and narrowed their lumina. The results of this study show that, in the terminal stages, cellular as well as gross morphologic differences exist between polycystic and medullary cystic kidney disease and that diphenylamine-induced cystic disease more closely resembles human polycystic than medullary cystic kidney disease.

Aniline Compounds↗
PubMed1991

Decreased incidence of diphenylamine-induced renal papillary necrosis in Syrian hamsters given dimethylsulphoxide.

The renal papillotoxicity of diphenylamine dissolved in dimethylsulphoxide (DMSO) was investigated in male Syrian hamsters, male Sprague-Dawley rats and female Mongolian gerbils. When diphenylamine in DMSO was administered orally to male Syrian hamsters (400, 600 or 800 mg/kg body weight/day for up to 9 days), the incidence of renal papillary necrosis was almost zero. Hamsters pretreated with DMSO (0.5 ml/100 g body weight/day) and 1 hr later given 400, 600 or 800 mg diphenylamine in peanut oil/kg body weight/day for 3 consecutive days had significantly reduced incidences of renal papillary necrosis (0/10, 0/10 and 1/10 in the low-, mid- and high-dose groups, respectively) when compared with hamsters given similar doses of diphenylamine but not pretreated with DMSO (5/10, 7/10 and 5/10 in the low-, mid- and high-dose groups, respectively). Focal, apex-limited renal papillary necrosis was observed in two Sprague-Dawley rats given 800 mg diphenylamine in DMSO/kg body weight/day orally for 9 days. Focal, intermediate renal papillary necrosis was observed in two additional rats administered 800 mg diphenylamine in DMSO/kg/day orally for 9 days. Renal papillary necrosis was not observed in any of the Mongolian gerbils. The results of these studies suggest that DMSO protects against diphenylamine-induced renal papillary necrosis in male Syrian hamsters.

Administration, Oral↗
PubMed1999

Diphenylamine as an important structure of nonsteroidal anti-inflammatory drugs to uncouple mitochondrial oxidative phosphorylation.

A marked difference has been observed in the inhibitory effects of nonsteroidal anti-inflammatory drugs (NSAIDs) on oxidative phosphorylation of rat liver mitochondria. It should be noted that some of the potent inhibitors, N-phenylanthranilic acids and diclofenac, have a similar "skeleton" structure, diphenylamine. Diphenylamine itself was found to inhibit oxidative phosphorylation significantly, although its inhibition potency was weaker than that of NSAIDs with a diphenylamine structure. In addition to decreases in the respiration control index (ratio of state 3 to state 4 respiration), these compounds released oligomycin-inhibited state 3 respiration. These results demonstrated that diphenylamine, as well as N-phenylanthranilic acids and diclofenac, was an uncoupler of oxidative phosphorylation of rat liver mitochondria. Thus, diphenylamine was suggested to play an important role in the uncoupling effects of NSAIDs with a diphenylamine skeleton.

Animals↗
PubMed2000

Possible mechanism of hepatocyte injury induced by diphenylamine and its structurally related nonsteroidal anti-inflammatory drugs.

Diphenylamine is a common structure of nonsteroidal anti-inflammatory drugs (NSAIDs) to uncouple mitochondrial oxidative phosphorylation and to cause a decrease in hepatocellular ATP content and hepatocyte injury. The mechanism for acute cell injury induced by diphenylamine and its structurally related NSAIDs was investigated with rat liver mitochondria and freshly isolated hepatocytes, focusing on the relation to the uncoupling of oxidative phosphorylation. Incubation of mitochondria with diphenylamine as well as mefenamic acid and diclofenac caused pseudoenergetic mitochondrial swelling, indicating that these compounds induce mitochondrial membrane permeability transition. Diphenylamine also caused changes in safranine-binding spectra to mitochondria that was energized by succinate oxidation. This spectral shift indicates the loss of mitochondrial membrane potentials, which is known as one of the characteristics for uncouplers of oxidative phosphorylation, and also was caused by mefenamic acid and diclofenac. Incubation of hepatocytes with mefenamic acid, diclofenac, and diphenylamine diminished cellular ATP content, followed by leakage of lactose dehydrogenase from hepatocytes. Fructose, a low K(m) substrate for glycolysis, partially protected against the ATP depletion and hepatocyte injury induced by these compounds. Further addition of oligomycin, which blocks ATPase, pronounced the protection against cell injury. These results suggested that decreases in cellular ATP content, mainly caused by uncoupling of mitochondrial oxidative phosphorylation, were responsible for acute hepatocyte injury induced by diphenylamine and structurally related NSAIDs.

Adenosine Triphosphate↗
PubMed2005

[Study on the inclusion interaction of water-soluble p-(N,N-dimethylamino)-calix[8]arene with diphenylamine-4-sulfonic sodium salt].

The inclusion interaction of water-soluble p-(N,N-dimethylaminomethyl)-calix[8]arene with diphenylamine-4-sulfonic acid sodium salt was investigated by fluorimetric method. When diphenylamine-4-sulfonic acid sodium salt was added into the p-(N,N-dimethylaminomethyl)-calix[8]arene solution, the emission spectrum of diphenylamine-4-sulfonic acid sodium salt occurred to a blue shift with the enhancement of the fluorescent intensity. The results show that the formation of the inclusion complex of the p-(N,N-dimethylaminomethyl)-calix[8]arene with diphenylamine-4-sulfonic acid sodium salt. The influence factors such as the pH value of solutions, solvents on the emission and excitation spectra of the inclusion complex were studied. It indicates that diphenylamine-4-sulfonic acid sodium salt penetrated the cavity of the calix[8]arene via the static action between the sulphonyl group of diphenylamine-4-sulfonic acid sodium salt and nitrogen atom of p-(N,N-dimethylaminomethyl)-calix[8]arene and the hydrophobic interaction of the aromatic rings.

Benzenesulfonates↗
PubMed1980

The function of diphenylamines as modifiers of photosystem II electron transport in isolated spinach chloroplasts.

Diphenylamines with highly electronegative substituents are effective inhibitors of photosynthetic electron transport and photophosphorylation. They inhibit only Photosystem II- and not Photosystem I-dependent photoreductions. As judged from the missing tetramethylphenylenediamine-bypass, displacement experiments with [14C]metribuzin, and measurements of oxygen evolution in trypsinated chloroplasts, diphenylamines act neither as dibromomethylisopropylbenzoquinone- nor as dichlorophenyldimethylurea-type inhibitors. All of the diphenylamines tested were found to function as ADRY-type reagents, (Renger, G. (1972) Biochim. Biophys, Acta 256, 428-439) which modify the stability of redox equivalents stored within the water-splitting enzyme system Y. The site of inhibition of diphenylamines is assumed to be located at the reducing side of Photosystem II or the reaction center itself. The inhibitory effect could involve a modification of cytochrome b-559 or its surrounding. In an assay for herbicidal activity, diphenylamines showed more pronouncing effect on mono- than on dicotyledonous plants.

Aniline Compounds↗
PubMed1985

[Determination of the number of somatic cells in milk using the rapid diphenylamine DNA filter method].

The rapid reaction of the diphenylamine agent with DNA was used for the determination of the counts of somatic cells in cow's milk, using the DNA filter method. The method is based on the filtration of a warmed (65-70 degrees C) mixture of milk with Triton X-100 through the Synpor nitrocellulose membrane filter, pore size 2 to 5 microns, and subsequent DNA determination of the collected somatic cells by the colour reaction of diphenylamine. A 2ml quantity of distilled water and 4 ml of diphenylamine reagent were added to the membrane filters with somatic cells. The mixture is warmed in water bath at 90 to 100 degrees C for 20 min., then it is cooled, centrifuged (3500 X g, 15 min.), and the optical density is measured at 595 nm. The relation 8 micrograms = 1 million cells was used for the conversion of DNA content to the counts of cells. The average variation coefficient of the determination was 5.9% and the coefficient of correlation between the diphenylamine DNA filter method and the direct microscopy of the somatic cells on membrane filters was r = 0.997. Using the diphenylamine DNA filter method, the counts of somatic cells can also be determined from milk samples stored in frozen condition or from the filters with collected cells kept at the temperature of 4 degrees C (10 days) or 25 degrees C (3 days). Milk stabilized with formaldehyde can also be used for the determination if stored at 4 degrees C.

Aniline Compounds↗
PubMed1989

Quantitation of total DNA per cell in an exponentially growing population using the diphenylamine reaction and flow cytometry.

The diphenylamine assay used to estimate the absolute mass of DNA/cell as well as absolute differences in DNA content between cell populations is based upon the assumption that all of the cells are in the G0 or G1 phase of the DNA synthetic cycle. However, if cells are in exponential growth and synthesizing DNA, portions of the population will be in S or G2 phases and the diphenylamine assay will overestimate the total mass of DNA/cell. Conversely, flow cytometry (FCM) can estimate relative differences in total DNA/cell and the proportions of an exponentially growing population in G1, S, and G2 but cannot estimate absolute mass or differences in DNA/cell. In this report, we describe a methodology of combined diphenylamine and FCM assays of total DNA/cell which is applicable to any eukaryotic cell population. The method involves using the two assay methods concurrently and correcting the diphenylamine data for the FCM-derived distribution of the cells within the DNA synthetic cycle. The methodology was tested on single-cell-derived stocks of the obligate intracellular protozoan parasite Trypanosoma cruzi which displays marked but stable intraspecific heterogeneity.

Animals↗
PubMed1987

Synthesis and biocidal activity of Zn(II) complexes of some 2,2'-substituted diphenylamines.

Binary as well as ternary complexes of Zn(II) with diphenylamine-2,2'-dicarboxylic acid (dpdc), diphenylamine-2-amino-2'-carboxylic acid (dpac), diphenylamine-2-hydroxy-2'-carboxylic acid (dphc), diphenylamine-2-mercapto-2'-carboxylic acid (dpmc), and N-(2-pyridino) anthranilic acid (npa) have been synthesized and characterized by their elemental analysis, IR spectral data, and molar conductance measurements. Antimicrobial activity of these ligands and their respective Zn(II) complexes have been determined on gram positive (Staphylococcus aureus) and gram negative (Escherichia coli) bacteria and on Aspergillus niger and Aspergillus nidulense, two common fungi by the serial dilution method. A considerable increase in the biocidal activity of these ligands on being coordinated with the metal ion has been reported in terms of their minimum inhibitory concentration (MIC) values.

Aniline Compounds↗
PubMed1993

Loss of the basement membrane matrix molecule, bamin, in diphenylamine-treated mice.

Polycystic kidney disease (PKD) is a life-threatening disease characterized by focal dilatations or cysts in certain kidney tubules. Changes (i.e. thickening) in the support structure for these tubules, the basement membrane, have been related to the development of the cysts. Analysis of changes in basement membranes of humans with PKD is difficult, however, due to the restricted amount of material available for study. Several genetic and induced animal models, including diphenylamine-treated rats, have been employed to study the effects of PKD on basement membrane synthesis. While all these studies agree that PKD has a significant influence on basement membranes, no clear understanding as to how PKD effects basement membrane composition has emerged. Here, we report our findings of the effect of diphenylamine treatment on the composition of the basement membrane. Our immunohistological studies indicate that bamin, a recently described glycoprotein associated with glomerular basement membranes (Robinson et al., 1989), is not present in the glomerular basement membranes of diphenylamine-treated mice. This finding was confirmed by analysis of the composition of the basement membrane matrix synthesized by EHS tumors grown in control and diphenylamine-treated mice. The possible role of bamin in the pathogenesis of renal cysts is discussed.

Animal Nutritional Physiological Phenomena↗