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At least 217 records · Page 12Linked to original sources
PubMed2002

9-(Trichloroacetylimino)acridine monohydrate.

The title compound, alternatively called N-acridin-9(10H)-ylidene-2,2,2-trichloroacetamide monohydrate, C(15)H(9)Cl(3)N(2)O.H(2)O, crystallizes in space group P2(1)/c with Z = 4. The acridine moieties are arranged in layers, tilted at an angle of 15.20 (4) degrees relative to the ac plane, while adjacent molecules pack in a head-to-tail manner. Acridine and water molecules form columns along the b axis held in place by a network of hydrogen bonds, which is the major factor stabilizing the lattice. The acridine molecule exhibits structural features of both the amino and imino forms, which could be due to the presence of the strong electronegative trichloroacetyl substituent at the exocyclic N atom.

Journal Article↗
PubMed1993

Photodynamic DNA strand breaking activities of acridine compounds.

Induction of single strand breaks in DNA was assessed by the conversion of supercoiled closed circular plasmid DNA into the open circular form. Euflavine produced single-strand breaks following irradiation but not in the control maintained in the dark. The single strand breaking activity of photoactivated euflavine was found to be dose-dependent. The effective dose conversion 50% (ED50) of the closed circular DNA to the open circular form was 0.53 microM. A comparison of 8 acridine compounds revealed that the ED50 of diaminoacridines such as euflavine, proflavine and acridine yellow or the 3,6-dimethylamino-derivative (acridine orange) was less than 1 microM while the ED50 values of the other acridines were greater than 80 microM. Euflavine was markedly inhibited by singlet oxygen scavengers such as NaN3, histidine, alpha-tocopherol or beta-carotene and partly inhibited by superoxide dismutase, mannitol or catalase. These results suggest that enflavine induces single strand breaks in DNA mainly by a type II photodynamic mechanism. Photodynamic single strand breaking activities appeared related to their mutagenic activities on yeast. This experimental system described here is useful for the quantitative assessment of the single strand breaking activities of various photosensitizers in vitro and for the determination of active oxygen species involved in those processes.

Acriflavine↗
PubMed1999

Pyrimido[4,5,6-kl]acridines. Synthesis, in vitro cytotoxicity and structure-activity relationships.

In a previous report we described the synthesis and biological properties of a group of pyrimido[4,5,6-kl]acridines 2, related to the pyrazolo[4,5,6-kl]acridines 1, promising antitumor agents possessing a broad spectrum of activity. Since the substitution of the pyrazole ring of the pyrazoloacridine chromophore with a pyrimidinone leads to derivatives that retain in vitro cytotoxic activity, we decided to further investigate the pyrimido[4,5 6-kl]acridines. Modifications at the ring system level, leading to chromophores with different characteristics, changes of substituent groups in position 6, simultaneous alteration of the chromophore and the introduction of a second cationic side chain in position 1 afforded 29 new pyrimido[4,5,6-kl]acridines, which were tested in vitro against the human colon adenocarcinoma HT29 cell line. Interesting structure-activity relationships could be drawn. Some selected derivatives were screened for their cytotoxic activity on the National Cancer Institute cell panel (60 human tumor lines).

Adenocarcinoma↗
PubMed2006

[Study on the inclusion behavior of p-sulphonatocalix[4]arene with acridine by spectrofluorometric titrations].

p-sulphonatocalix[4] arene (1) was prepared according to the literature, and spectrofluorometric titrations were performed to investigate the inclusion behavior of (1) and acridine in citrate buffer solution (pH 5.92, 0.1 mol x L(-1)) at different temperatures. It was found that in definite concentration range, the emission peak of acridine exhibited a slight red shift and th fluorescence intensity decreased when (1) was added. They form stable host-guest complex, and the stoichiometry of the inclusion complex is 1 : 1. The stability constants of the inclusion complex at 15.0 degrees C, 20.0, 25.0 and 30.0 degrees C were determined as 3.08 x 10(5), 4.45 x 10(4), 2.58 x 10(4) and 8.90 x 10(3), respectively. The thermodynamic parameters of inclusion process, deltaG, deltaH and deltaS, were determined. The experimental results indicated that the inclusion process was an exothermic and enthalpy-driven process. It was found that the stability constants descended when temperature rose. The most probable pattern of the inclusion complex between (1) and acridine was proposed as: acridine partially goes into the cavity of (1), and the protonated N atom and the negatively charged sulphonyl group bond firmly owing to strong electrostatic interaction. With the main contribution of electrostatic interaction and the assistance of Van de Waals and hydrophobic interaction, the host and the guest molecules form 1 : 1 supramolecular complex.

English Abstract↗
PubMed1980

Acridine orange-nucleic acid fluorescence. Its use in routine diagnostic muscle biopsies.

Acridine orange-RNA fluorescence in diagnostic muscle biopsies is a sensitive, specific method to identify single fibers undergoing neurogenic atrophy. Fibers thus identified may be clearly distinguished from nonfluorescent type-specific atrophic fibers, as well as from atrophic fibers encountered in other myopathic conditions. Regenerating fibers, inflammatory cells, and mast cells stain prominently with acridine orange but area easily identified by their morphologic features. Acridine orange-RNA fluorescence is extremely useful in the evaluation of early neurogenic atrophy without fiber-type grouping and may be performed on paraffin-embedded sections, thus allowing retrospective studies. In addition, this technique may provide clues to the pathogenesis of neuromuscular disease that involves altered nucleic acid metabolism.

Acridine Orange↗
PubMed1996

Drug metabolizing enzyme induction by benzoquinolines, acridine, and quinacrine; tricyclic aromatic molecules containing a single heterocyclic nitrogen.

Rats were treated with nitrogen-containing phenanthrene (3,4-, 5,6-, or 7,8-benzoquinoline) or anthracene (acridine or quinacrine) derivatives at a dose of 75 mg/kg, daily for 3 days. The hepatic drug metabolizing enzyme response ranged from no induction (quinacrine) through low (5,6-benzoquinoline), intermediate (acridine), and high (3,4-benzoquinoline) magnitude increases of only phase II enzymes, to induction of both phase I and phase II enzymes (7,8-benzoquinoline). The phase I enzyme response of 7,8-benzoquinoline was an induction of CYP1A. All three benzoquinolines, but neither anthracene derivative, elevated NAD(P)H quinone oxidoreductase activity. A similar pattern but of lesser magnitude was seen with glutathione S-transferase activity. 3,4-Benzoquinoline was the only agent to significantly increase microsomal epoxide hydrolase activity (2,3-fold). Both 3,4- and 7,8-benzoquinoline increased UDP-glucuronosyltransferase activity toward 4-nitrophenol (40% and 70%, respectively), but only the 3,4-isomer increased activity toward morphine (75%), diclofenac (75%), and testosterone (23%), and only the 7,8-isomer increased activity toward chloramphenicol (105%). 3,4-Benzoquinoline elevated the hepatic mRNA concentration of UGT2B1 but not UGT1*6. Acridine treatment increased UDP-glucuronosyltransferase activity toward morphine (47%), 1-naphthol (28%), testosterone (19%), and estrone (19%). Quinacrine failed to elevate any UDP-glucuronosyltransferase activity and depressed activities toward testosterone and estrone by 20%. This study shows that some tricyclic aromatic compounds containing a single heterocyclic nitrogen atom have the potential for use as chemoprotective agents based upon their ability to selectively induce only phase II enzymes.

Acridines↗
PubMed1982

[The fluorescent staining of mitochondria in living HeLa- and LM-cells with new acridine dyes (author's transl)].

The fluorescent staining of mitochondria in living cells with new acridine dyes is reported. The fluorescent dyes used are derivatives of acridine orange (AO) and of 3-amino-6-methoxyacridine (AMA) with various residues in 9- or 10-position (Scheme 1). They are either permanent cationic dyes or cations which are formed by protonation in the culture medium. HeLa cells and mouse fibroblasts (LM cells) have been used for our staining experiments. On favourable conditions we succeeded in staining the mitochondria not only orthochromatically but also metachromatically. Photodynamical effects which have been observed during the exposure of the stained cells in the fluorescence microscope are described. The residues in 9- or 10-position favour the dye accumulation in the mitochondria. Vital staining with the basic compounds AO and AMA however leads to the formation of metachromatically stained lysosomes in the orthochromatically stained cytoplasm. The dye 3-amino-6-methoxy-9-(2-hydroxyethyl)acridine stains the nucleus of living cells.

Acridine Orange↗
PubMed1980

Further studies on the nature of red fluorescent structures in neuroblastoma monolayer cells vitally stained with acridine orange.

The nature of red fluorescent particles in vitally acridine orange stained C 1300 neuroblastoma monolayer cells was evaluated by electron microscopy, cytofluorometry, cytopharmacological and cell fractionation studies. At the ultrastructural level the distribution of red fluorescent granules correlated with that of the Golgi complex and Golgi derived structures during various stages of differentiation, mitosis, and under colcemid treatment. Cytopharmacological studies revealed that red fluorescence was displaced in a concentration and time dependent manner with the basic drugs chloroquine and quinacrine. Subcellular fractionation studies showed that acridine orange was concentrated in fractions that also contained the highest amount of acid phosphatase and electron dense vesicles. Vital acridine orange staining of neuroblastoma cells in culture can give information on the relationship between Golgi-derived vesicles and cell functions like proliferation and differentiation. The influence of drugs on these processes can be studied.

Acid Phosphatase↗
PubMed1982

[Fluorescent staining of chromosomes and nuclear structures in living LM- and HeLa-cells with new acridine dyes].

Fluorescent staining of chromosomes and nuclear structures (nucleolus associated chromatin) in living HeLa- and LM-cells (mouse fibroblasts) with new acridine dyes is reported. The dyes have aminoethylgroups in 9-position with different end groups at this residue (scheme of structures). Dyes without these 9-substituents only induce the formation of lysosomes. An exceptional position on vital staining of chromosomes and nuclear chromatin has the dye 3-amino-6-methoxy-9-(2-hydroxyethylamino)acridine 1. Concentrations of 10(-3) M can be used in vital staining experiments. Measuring the consumption of oxygen we could demonstrate that the dye has no effect on the activity of respiration even at these high dye concentrations. Therefore we conclude that we have really observed vital staining and not postvital staining of chromosomes and nuclear chromatin. Similar properties has the well known vital dye acridine orange.

Acridines↗
PubMed1976

Some quantitative aspects of Acridine Orange fluorescence in unfixed, sucrose-isolated mammalian nuclei.

Nuclei were isolated from mouse liver and central nervous system (CNS). These nuclei were fluorochromed without fixation in a 0.25 M sucrose medium containing 5-5 X 10(-5) M Acridin Orange and measured with an incident microfluorometric system. In the case of mouse CNS nuclei, the major and minor axes of the nuclei were measured with a filar micrometer. Three modal values were obtained from the hepatocyte suspension corresponding to 2C, 4C, and 8C nuclei, respectively. While the CNS nuclei displayed substantial variability in size, the Acridine Orange emission values at 530 nm were nearly constant. The data suggest that under these conditions, Acridine Orange fuorescence reflects DNA content. Further, the 530 nm fluorescence emission is not affected by chromatin condensation or proteins complexed with DNA.

Acridines↗
PubMed1990

The reaction of acridine orange with proteoglycans in the articular cartilage of the rat.

Acridine Orange in concentrations from 0.01% to 0.2% was added to the first fixative solution in order to stain vibratome sections and small blocks of the articular cartilage of 2 month old rats. The interterritorial matrix of the radial or deep zone (zone 3) was examined. It contained reaction products with different morphology depending on the specimens used. In vibratome sections filaments were seen arranged in a homogenous pattern and changing in size with the concentration of the dye: diluted solutions produced finer filaments than concentrated ones. In contrast, in tissue blocks the staining pattern was not altered by different concentrations of Acridine Orange. However, with increase of the distance from the surface of the specimens the size of the filaments gradually decreased and formed a finer network. Since after preincubation with chondroitin ABC lyase only minute reaction products remained, an interaction of the dye with the sulphated glycosaminoglycans of the proteoglycans in the articular cartilage is suggested. The experiments show that by using mainly monocationic monomers of Acridine Orange the proteoglycans can be stained in a more expanded state than with polycationic dye polymers.

Acridine Orange↗
PubMed1982

Acridine orange staining of smears for demonstration of Mycobacterium tuberculosis.

Acridine orange staining for the detection of mycobacteria was compared with staining by auramine O and with mycobacterial culture in a series of 1071 clinical specimens. A total of 78 (7%) specimens were positive by staining. No false positive or negative findings were recorded by the acridine orange method. The two fluorochromes proved equal in their ability to detect mycobacteria in specimens from culture positive cases of tuberculosis. In the rapid bacteriological diagnosis of tuberculosis, acridine orange offers a good alternative to auramine O which is considered carcinogenic.

Acridine Orange↗
PubMed2002

Effect of structure on antibiotic action of new 9-(ethylthio)acridines.

Six new 9-(ethylthio)acridine derivatives were examined for antibacterial and antifungal activities with 10 bacterial and 8 yeast strains. The only active compounds were 2- and 3-amino derivatives. The observed MICs (mg/L) for 2-amino-9-(ethylthio)acridine (possessing the highest biological activity) were 12 (P. mirabilis), 30 (B. subtillis), 60 (C. freundii), 90 (E. coli), 128 (E. vulneris) and 500 (S. marcescens and S. aureus). Both amino derivatives have also lowest half-wave potential (E1/2) and field Swain-Lupton constants (describing oxidoreduction behavior) what supports the importance of acridine ion formation in the mechanism of antimicrobial action.

Acridines↗
PubMed1983

Apparent inhibition of Na+/H+ exchange by amiloride and harmaline in acridine orange studies.

Amiloride and harmaline were tested as inhibitors of proton movements in brush-border membrane vesicles from rat kidney cortex. Transmembrane pH differences were visualized using acridine orange. Fluorescence quenching due to Na+ gradient-driven intravesicular acidification was inhibited by amiloride and harmaline. However, a similar inhibition was observed for the Na+ gradient-driven electrogenic proton movements in the presence of gramicidin. Moreover, amiloride and harmaline decreased the fluorescence signal of electrogenic proton movements driven by a K+ gradient in the presence of valinomycin. The degree of inhibition of intravesicular acidification by both drugs was concentration dependent. Half-maximal inhibition (I50) of Na+/H+ exchange and K+ gradient-driven proton movements occurred at 0.21 and 0.6 amiloride, respectively. The I50 for harmaline was 0.21 mM in both cases. Amiloride also decreased the initial quenching of acridine orange fluorescence due to a preset pH gradient without affecting the rate of dissipation of the pH gradient. This effect was independent of the buffer capacity. In contrast, harmaline seemed to dissipate pH gradient in the same way as a permeant buffer. Amiloride and harmaline led to a concentration-dependent fluorescence decrease even in aqueous solution. The results suggest an interaction of amiloride and harmaline with acridine orange which overlaps a possible specific inhibition of Na+/H+ exchange by these drugs.

Acridine Orange↗
PubMed1977

Interaction of acridines and tetrahydroacridines with DNA at low DNA/dye ratios.

This study examines certain aspects of the interaction of acridines with DNA. A comparative study of the methods available for the determination of the association constants (Kap) for compounds which interact with DNA has been pursued. A new equation which permits the spectrophotomeric determination of Kap has been derived. This equation can be applied to compounds which upon interaction with a polymer exhibit discrete absorption changes. Application of this equation to substituted acridines and tetrahydroacridines yields some preliminary information on the effect of ring substituents on the interaction of acridines with DNA. Low levels of DNA/dye ratios have been used in the studies reported herein.

Acridines↗
PubMed1989

10-N nonyl-acridine orange: a fluorescent probe which stains mitochondria independently of their energetic state.

The specificity of binding of 10-N Nonyl Acridine Orange to mitochondria, and more precisely to inner membranes, is demonstrated by subcellular fractionation of hepatocytes. Unlike Rhodamine 123, which is a preferential marker of the transmembrane potential, Nonyl Acridine Orange binding is essentially independent of the mitochondria energization state although a low uptake of this dye, in response to the potential, may be measured. So 10-N Nonyl acridine orange is an appropriate marker of the mitochondial membrane surface per unit of cell mass.

Acridine Orange↗
PubMed1992

Selective binding to AT sequences in DNA by an acridine-linked peptide containing the SPKK motif.

The sequence selectivity of binding to DNA by an acridine-linked peptide ligand has been investigated by means of footprinting methodologies. The ligand conjugates an anilino-acridine intercalating chromophore with the potentially minor groove binder octapeptide SPKKSPKK. This basic peptide corresponds to a highly conserved DNA recognition motif found in histone H1 and several other nonhistone proteins. Three complementary techniques using DNase I, hydroxyl radicals and osmium tetroxide as sequencing probes have been employed to evaluate both the sequence specificity of binding and the drug-induced conformational changes in DNA. The results converge to demonstrate the AT-selectivity and support a model in which the peptide moiety lies in the minor groove. DNA-binding sites of the conjugate are restricted to a few alternating AT-sequences proximal to GC-rich regions. Binding to homooligomeric runs of A and T is clearly disfavoured by the hybrid whereas such sequences represent preferred binding sites for the unsubstituted basic peptide. These differences reflect the influence of the anilino-acridine chromophore, which evidently contributes to the DNA recognition process allowing the peptide only to contact defined DNA sequences.

Acridines↗
PubMed1980

Acridine structure correlated with mutagenic activity in Salmonella.

The structural basis for direct mutagenicity of acridines was studied by testing 50 different analogs in the Ames Salmonella tester strains without the addition of mammalian activating enzymes. These experiments showed that the single most effective substituent for frameshift mutagenesis in strain TA1537 is an amino group at the "9" position, while an amino group at either the "3" or "1" position is less effective. Other substitutions at the "9" position demonstrate decreased frameshifting activity compared to 9-aminoacridine. Furthermore, all substituents in combination with the amino group of 9-aminoacridine also decrease frameshifting activity, except for the addition of another amino group at the "1" position or a methyl at the ring nitrogen. Nitro substituents at the "1" and "3" positions enhance 9-aminoacridine toxocity. All nitro substituents decrease typical acridine-frameshift mutagenesis for strain TA1537, but they induce mutagenic activity either in the other type of frameshift strain, TA1538, or in the base-pair substitution strain TA1535. These studies have provided important structure-function relationships for acridine mutagenicity and toxicity in Salmonella. Consequently, this biological system has provided a sensitive means for determining the structural requirements for mutagenic mechanisms.

Acridines↗