Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Ninhydrin”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 37 records · Page 2Linked to original sources
PubMed1997

Rhinitis caused by ninhydrin develops into occupational asthma.

Ninhydrin (2,2-dihydroxy-1,3-indanedione or 1,2,3-triketo-hydrindene hydrate) is a chemical used in the detection of free amino and carboxyl groups in proteins and peptides. Allergic, immunoglobulin E (IgE)-mediated rhinitis caused by ninhydrin was diagnosed earlier in a 41 yr old woman working as a laboratory technician in a forensic laboratory. Despite handling ninhydrin only in a flow cabinet, symptoms of dyspnoea developed 6 months later. Peak flow was found to vary by 20% during working days. In the specific inhalation challenge it was shown that occupational asthma had also developed due to continuing slight exposure to ninhydrin. The titre of ninhydrin-specific IgE also increased from 0.6 to 1.1 kU x L(-1) in the follow-up. This case stresses the importance of cessation of allergen exposure in occupational allergic rhinitis, in order to prevent asthma.

Adult↗
PubMed2002

Advanced solvent-free application of ninhydrin for detection of latent fingerprints on thermal paper and other surfaces.

This work presents the first known experiments of ninhydrin sublimation in vacuum to detect latent fingerprints on thermal paper. In this method, latent fingerprints become visible in rich detail without the background black staining known from the application of ninhydrin solutions to thermal paper. The method involves hanging the thermal paper samples 15 cm above a heating source with dispersed ninhydrin crystals in a vacuum chamber. The optimized conditions for ninhydrin sublimation are 50 mg ninhydrin, 2 to 5 mbar vacuum, and 150 degrees C heating source temperature for 30 min. The application of this method is also successful on the new euro notes. Latent fingerprints can be developed across the transitions from paper to optical variable device (OVD).

Journal Article↗
PubMed2004

Ninhydrin treatment as a screening method for the suitability of swabs taken from contact stains for DNA analysis.

More and more swabs containing unknown traces of biological material are submitted for forensic DNA analysis. Most of the samples are swabs taken from handled items such as tools, weapons and handles etc. Therefore, we tried to develop a screening method in order to focus the investigation on samples containing biomolecules, such as amino acids which might be associated with nucleic acids. A total of 285 swabs taken from various items collected during crime scene investigations were treated with ninhydrin which leads to a purple colour for samples containing amino acids. Of the swabs 158 were classified as ninhydrin positive and 76% of these samples yielded DNA profiles that fulfil the criteria for inclusion in the German national DNA database (profile frequency greater than 1 in 100,000) or in DNA mixtures which could at least be compared with suspects. In comparison only 9% of the 127 samples shown to be ninhydrin negative, revealed a usable DNA profile. Consequently, ninhydrin treatment was found to be an effective screening method which resulted in an increase in the rate of successfully typed samples and subsequently in a reduction of the costs due to the lower number of samples that needed to be typed.

DNA Fingerprinting↗
PubMed1991

Thiol-group reactivity, hydrophilicity and stability of alloxan, its reduction products and its N-methyl derivatives and a comparison with ninhydrin.

The diabetogenic agent, alloxan, is a hydrophilic and chemically unstable compound. The logarithm of the octanol/water partition coefficient of alloxan was found to be -1.86; its half-life at pH 7.4 and 37 degrees in phosphate buffer was 1.5 min. The partition coefficients and half-lives of the alloxan reduction products, alloxantin and dialuric acid, were very similar to those of the parent compound; N-methylalloxan and N,N'-dimethylalloxan were less hydrophilic but more unstable. Ninhydrin was found also to be hydrophilic although this compound, in contrast to alloxan and its derivatives, was quite stable in aqueous solution. Alloxan and its N-methyl derivatives were reduced by thiols and in the presence of glutathione and cysteine, rapid redox cycling occurred, with formation of 'active oxygen' species; no such reaction was observed, however, with ninhydrin. Comparatively slow redox cycling was recorded with alloxan derivatives and dithiothreitol although rapid cycling occurred with ninhydrin and this dithiol. Such differences may explain why ninhydrin does not share with alloxan a selective toxic effect upon the pancreatic B-cell.

Alloxan↗
PubMed2004

Ninhydrin-dyed latent fingerprints as a DNA source in a murder case.

In this case report, we describe the possibility of using ninhydrin-dyed fingerprints as a DNA source for STR typing. Preliminary tests prove that ninhydrin-dyed material still can be useful for STR typing. The case material consisted of seven ninhydrin-labeled latent fingerprints found at a murder crime site, which could not be typed in a classical manner. We were able to swap DNA from the ninhydrin-treated areas and successfully use it for STR typing.

DNA↗
PubMed2005

The development of novel ninhydrin analogues.

Following its discovery by Siegfried Ruhemann in 1910, ninhydrin rapidly became a practical analytical tool. In 1954 it was found to be an important reagent to develop fingerprints on porous surfaces. Since its use in forensic chemistry, many efforts have focused on improving the reagent. Many of the shortcomings of ninhydrin have been met by the synthesis of a variety of ninhydrin analogues. This tutorial review provides a short introduction to ninhydrin and highlights the different synthetic approaches used in the development of analogues for the detection of latent fingerprints.

Forensic Medicine↗
PubMed1997

Comparative toxicity of alloxan, N-alkylalloxans and ninhydrin to isolated pancreatic islets in vitro.

The in vitro toxicity of the diabetogenic agent alloxan as documented by the induction of beta cell necrosis was studied in isolated ob/ob mouse pancreatic islets. The effect of alloxan has been compared with that of a number of N-alkyl alloxan derivatives and with that of the structurally related compound, ninhydrin. Alloxan and its derivatives were selectively toxic to pancreatic beta cells, with other endocrine cells and exocrine parenchymal cells being well preserved, even at high concentration. In contrast, ninhydrin was selectively toxic to pancreatic beta cells only at comparatively low concentration, destroying all islet cell types at high concentrations. The ultrastructural changes induced by all the test compounds in pancreatic beta cells in vitro were very similar to those observed during the development of alloxan diabetes in vivo. The relative toxicity of the various compounds to pancreatic beta cells in vitro was not, however, related to their ability to cause diabetes in vivo. Indeed, the non-diabetogenic substances ninhydrin, N-butylalloxan and N-isobutylalloxan were very much more toxic to isolated islets than the diabetogenic compounds alloxan and N-methylalloxan. These results suggest that the differences in diabetogenicity among alloxan derivatives are not due to intrinsic differences in the susceptibility of the pancreatic beta cells to their toxicity, but may reflect differences in distribution or metabolism. High concentrations of glucose protected islets against the harmful effects of alloxan and its derivatives, but not those of ninhydrin. Low levels of glucose, and non-carbohydrate nutrients, afforded little protection, indicating that the effect of glucose is not due to the production of reducing equivalents within the cell, 3-O-Methylglucose, which protects against alloan diabetes in vivo, did not protect against alloxan toxicity in vitro. Since 3-O-methylglucose is known to prevent uptake of alloxan by pancreatic beta cells, it appears that uptake of alloxan by the cell is not a prerequisite for the induction of beta cell necrosis.

Alloxan↗
PubMed1980

[GABA fluophore formation due to ninhydrin reaction in the octanolic milieu. Spectrofluorometric investigation. 2nd information (author's transl)].

As a result of the reaction of ninhydrin with gamma-aminobutyric acid and glutamic acid in the octanolic milieu, a fluorescent product, presumably a copper-II-chelate-complex, was formed. Partial reaction steps were investigated spectrofluorometrically. The excitation and emmission spectra resulting from the reaction between ninhydrin and glutamic acid, ninhydrin and gamma-aminobutyric acid, and ninhydrin, glutamic acid and gamma-aminobutyric acid were measured. Possible consequences are discussed with respect to fluorescence histochemical procedures.

Copper↗
PubMed1980

Modification of hemoglobin by ninhydrin.

The Strecker degradation reaction was evaluated as a means of modifying hemoglobin in vitro, utilizing ninhydrin as a model compound. Ninhydrin led to modification of hemoglobin (when incubated with hemoglobin or red cells) at physiologic temperature and pH. Isoelectric focusing documented the formation of new hemoglobin bands, all with decreased (more negative) isoelectric points that hemoglobin A. Both alpha and beta chains were modified to an equal degree, although electrophoretic studies documented two modified species of alpha-chains and three modified species of beta-chains. Amino acid analysis of modified hemolysate following NaB3H4 reduction revealed peaks that coeluted with deaminated valine, epsilon-deaminated lysine, and a product with the guanidino group of arginine. The oxygen affinity of hemoglobin increased following its incubation with increasing concentrations of ninhydrin. These studies suggest that ninhydrin is representative of a class of carbonyl compounds that could be utilized to specifically modify that structure and function of hemoglobin variants.

Chemical Phenomena↗
PubMed1989

Ultrastructural cytochemistry of hepatic lysosomes and their protein components is selectively revealed by the ninhydrin-dimethyl sulfoxide-thiocarbohydrazide-silver proteinate reaction.

Proteins in lysosomal membranes, lysosomes and within the transtubular network are readily accessible for electron microscopic analysis by a new three-step method. Oxidative deamination of tissue-bound amino acids by ninhydrin in aqueous dimethyl sulfoxide and the concomitant formation of corresponding carbonyl groups comprise the first step. The addition reaction of thiocarbohydrazide to tissue-bound carbonyl groups comprises the second step, while the reduction of silver proteinate by tissue-bound thiocarbohydrazones is the final step of this sequential method. Glutaraldehyde-fixed and osmified ultrathin sections of rat liver embedded in LR White were oxidatively deaminated for 24 h by 1% w/v ninhydrin in aqueous 75% v/v dimethyl sulfoxide (DMSO). They were then incubated for 40 min in aqueous 1% w/v thiocarbohydrazide (TCH) and stained for 30 min at 50 degrees C with silver proteinate (SP). The ninhydrin-dimethyl sulfoxide-thiocarbohydrazide-silver proteinate (N-DMSO-TCH-SP) reaction proved to be chemically specific and highly selective for ultrastructural resolution of the internal structure of lysosomes and their protein components. We conclude that the N-DMSO-TCH-SP reaction is the method of choice for cytochemical elucidation of the protein ultrastructure of lysosomes and their enzymatic aggregates.

Animals↗
PubMed1989

Direct determination of bound sialic acids in sialoglycoproteins by acidic ninhydrin reaction.

A simple and rapid method for sialic acid determination in sialoglycoproteins by acidic ninhydrin reaction is described. The method is based on the reaction of sialic acids with an acidic ninhydrin reagent (K. Yao and T. Ubuka (1987) Acta Med. Okayama 41, 237-241). By heating a sample solution containing sialoglycoprotein with the reagent at 100 degrees C for 10 min, a stable color with an absorption maximum at 470 nm was produced. The standard curve was linear in the range of 20 micrograms to 3 mg of fetuin, a sialoglycoprotein, per 3.0 ml of the reaction mixture. The reaction is specific only for sialoglycoproteins among various proteins examined. The acidic ninhydrin method was applied to the determination of sialic acids in sialoglycoproteins in ascites fluids of Ehrlich ascites tumor-bearing mice.

Animals↗
PubMed1993

Monitoring tripeptidase activity using capillary electrophoresis. Comparison with the ninhydrin assay.

Capillary electrophoresis (CE) was used to assay the activity of a tripeptidase from a crude extract of Lactococcus lactis subsp. lactis NCDO 712 against the substrate, Gly-Gly-Phe and a comparison with a standard ninhydrin assay was made. Standard curves of the substrates and products showed a significantly variable colorimetric reaction to ninhydrin making accurate quantification of the tripeptidase problematic. The CE assay further demonstrated that the presence of contaminating enzymes in crude cell-free extracts can cause secondary reactions that are not apparent from the ninhydrin assay data. The CE assay was also able to generate enzyme kinetics data and monitor, during purification, the presence of co-eluting contaminating activities. The speed and sensitivity with CE allows routine analysis of the tripeptidase activity without any derivatization normally required for this enzyme.

Amino Acid Sequence↗
PubMed1992

Assay of sialidase activity using ion-exchange chromatography and acidic ninhydrin reaction.

A new assay method for sialidase (EC 3.2.1.18) activity using ion-exchange chromatography and acidic ninhydrin reaction has been developed. Fetuin, 4-methylumbelliferyl-N-acetylneuraminic acid (MUB-NANA), gangliosides and N-acetylneuramin-lactose were examined as substrates. Free sialic acid liberated from these substrates by sialidase reaction was isolated with a Dowex 1-X8 column (trifluoroacetate form, 1.5 cm x 0.5 cm I.D.) and determined by acidic ninhydrin reaction. Among the substrates tested, MUB-NANA was the best in the present method, N-Acetylneuramin-lactose could not be used as the substrate, because it was not separated from liberated sialic acid under the conditions used. The recovery of N-acetylneuraminic acid was above 88%, and the sensitivity of the method was 20 nmol in 300 microliters of the reaction mixture. The method was applied to the sialidase assay during its purification from rat skeletal muscle, and a Michaelis constant of 1.15 mM was obtained with MUB-NANA as the substrate. The method using the acidic ninhydrin reaction was simple and exhibited good reproducibility.

Animals↗
PubMedDate not supplied

Rapid shape change and release of ninhydrin-positive substances by Leishmania major promastigotes in response to hypo-osmotic stress.

Leishmania major promastigotes were grown to late-log phase and washed and resuspended in an isosmotic buffer. When osmolality was suddenly decreased by 50%, the cells rapidly became shorter and increased in width. Cell volume, calculated assuming a prolate-ellipsoidal shape, increased 1.4 times after 1 min. Over the next several minutes, the average length and width returned to control values while the volume returned to baseline, indicating the ability to regulate volume. Concomitantly with the swelling, large amounts of alanine and other ninhydrin-positive substances were released. All of the alanine pool was released within 1 min after reduction of the osmolality by 66%. Cells pre-loaded with [14C]-aminoisobutyric acid also released it very rapidly upon hypo-osmotic stress. Release of ninhydrin-positive substances resulted from decreased osmolality rather than changes in ionic composition. The same results were obtained if osmolality was decreased by reducing only the NaCl content of the buffer instead of diluting it with water, and mannitol could substitute for the NaCl. Promastigotes were able to grow well over several days in media as low as 154 mOsm/kg. The nature of the signalling mechanisms(s) that initiates the rapid shape change and efflux of ninhydrin-positive substances in response to hypo-osmotic stress is at present unknown.

Alanine↗
PubMed1986

Rubidium uptake by mouse pancreatic islets exposed to 6-hydroxydopamine, ninhydrin, or other generators of hydroxyl radicals.

The purpose was to study the toxicity of drugs known to generate free radicals on isolated pancreatic islets. The accumulation of 86Rb+ by mouse pancreatic islets was measured in vitro. Exposing the islets to 6-hydroxydopamine, ninhydrin, or phenazine methosulphate+NADH inhibited the Rb+ uptake, whereas paraquat or acetylphenylhydrazine had no effect. This effect of 6-hydroxydopamine was prevented by either of the hydroxyl radical scavengers, sodium benzoate and mannitol, but not by the non-scavenger, urea; ninhydrin was partially protected against by mannitol but not by benzoate. Protection against 6-hydroxydopamine was also afforded by D-glucose but not by L-glucose or 3-O-methyl-D-glucose; none of the sugars protected against ninhydrin. In damaging islet beta-cells and in being protected against by D-glucose, 6-hydroxydopamine closely resembles the diabetogenic drug, alloxan. It is suggested that protection against alloxan may involve both glucose metabolism and the interaction of glucose with its membrane-located carrier, while protection against 6-hydroxydopamine appears to be unrelated to the hexose carrier mechanism.

Animals↗
PubMed1990

Alloxan and ninhydrin inhibition of hexokinase from pancreatic islets and tumoural insulin-secreting cells.

Alloxan inhibited hexokinase activity in cytoplasmic fractions of transplantable radiation-induced rat islet cell tumours, ob/ob mouse pancreatic islets, rat liver and rat kidney. Half maximal inhibitory concentrations of alloxan were greater than those previously found for half maximal inhibition of pancreatic islet or liver glucokinase. D-glucose, preferentially the alpha-anomer, and D-mannose protected hexokinase activity against alloxan inhibition. 1,4-Dithiothreitol completely protected against and partially reversed the alloxan inhibition of hexokinase. The ability of various dithiols to reverse the inhibition of hexokinase by alloxan was dependent on the spacing between the SH (thiol) groups. Only dithiols with intermediate spacing between the SH groups were effective. Dithiols with two vicinal SH groups such as 1,2-dimercaptoethane and 2,3-dimercaptopropanol (BAL) and dithiols with more widely spaced SH groups such as 1,5-dimercaptopentane were ineffective. Thus a reaction of alloxan with two SH groups in the sugar binding site of the hexokinase with the formation of a disulfide bond may be involved in the reversible inhibition of the enzyme. Ninhydrin also inhibited hexokinase from all four tissues studied. The half maximal inhibitory concentrations of ninhydrin were lower than those of alloxan. Inhibition of hexokinase may be an important factor in the general cytotoxic action of ninhydrin. However, inhibition of pancreatic islet hexokinase is unlikely to be the initial event in the pancreatic B-cell toxic action of alloxan, even if inhibition of hexokinase by high concentrations of alloxan may contribute to the B-cell toxic action.(ABSTRACT TRUNCATED AT 250 WORDS)

Alloxan↗
PubMed1987

Determination of sialic acids by acidic ninhydrin reaction.

A new acidic ninhydrin method for determining free sialic acids is described. The method is based on the reaction of sialic acids with Gaitonde's acid ninhydrin reagent 2 which yields a stable color with an absorption maximum at 470 nm. The standard curve is linear in the range of 5 to 500 nmol of N-acetylneuraminic acid per 0.9 ml of reaction mixture. The reaction was specific only for sialic acids among the various sugars and sugar derivatives examined. Some interference of this method by cysteine, cystine and tryptophan was noted, although their absorption maxima differed from that of sialic acids. The interference by these amino acids was eliminated with the use of a small column of cation-exchange resin. The acidic ninhydrin method provides a simple and rapid method for the determination of free sialic acids in biological materials.

Chemical Phenomena↗
PubMed2004

Cyanide reaction with ninhydrin: elucidation of reaction and interference mechanisms.

A new sensitive spectrophotometric method has recently been developed for the trace determination of cyanide with ninhydrin. Cyanide ion was supposed to act as a specific base catalyst. Nevertheless, this paper demonstrates that the reported assay is based on a novel reaction of cyanide with 2,2-dihydroxy-1,3-indanedione, which affords purple or blue colored salts of 2-cyano-1,2,3-trihydroxy-2H indene. Hydrindantin is merely an intermediary of the reaction. The formation of a stable and isolable ninhydrin-cyanide compound has been confirmed by its preparation in crystalline form. Also, it is thoroughly characterized by elemental as well as MS, IR, UV/VIS and 1H NMR analyses. The Ruhemann's sequence of reactions of cyanide with ninhydrin has been reconsidered and an adequate mechanism of the reaction is proposed. As a consequence, the interference of oxidizers as well as copper, silver and mercury ions with the cyanide determination has been elucidated.

Cyanides↗