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Results for “ACRIDINE DYES”

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At least 19 recordsLinked to original sources

PubMed2004

Fluorescence of acridinic dyes in anionic surfactant solution.

The interaction of the cationic dyes acridine, 9-aminoacridine (9AA), and proflavine, with sodium dodecyl sulfate (SDS) was studied by electronic absorption, steady-state and time-resolved fluorescence spectroscopies. The dyes interact with SDS in the pre-micellar region leading in two cases to dimerization in dye-surfactant aggregates, but with distinct molecular arrangements. For proflavine, the observed red shift of the electronic absorption band indicates the presence of J-aggregate, which are nonfluorescent. In the case of 9AA, the aggregates were characterized as nonspecific (neither J- nor H-type is spectroscopically observed). The time-resolved emission spectra gives evidences of the presence of weakly bound dimers by the recovery of three defined decay times by global analysis: dye monomer (tau1 = 16.4 ns), dimer (tau2 = 7.1 ns), and a faster component (tau3 = 2.1 ns) ascribed to intracluster energy migration between monomer and dimer. Acridine has a weak interaction with SDS forming only an ion pair without further self-aggregation of the dye.

Acridines↗

PubMed2003

Excited state characteristics of acridine dyes: acriflavine and acridine orange.

The magnitude of the Stokes shift (frequency shifts in absorption and fluorescence spectra) is observed on changing the solvents and further has been used to calculate experimentally the dipole moments (ground state and excited state) of acriflavine and acridine orange dye molecules. Theoretically, dipole moments are calculated using PM 3 Model. The dipole moments of excited states, for both molecules investigated here, are higher than the corresponding values in the ground states. The increase in the dipole moment has been explained in terms of the nature of the excited state. Acriflavine dye overcomes the non-lasing behaviour of acridine orange due to quaternization of the central nitrogen atom.

Acridine Orange↗

PubMed1987

Oxygen radicals mediate cell inactivation by acridine dyes, fluorescein, and lucifer yellow CH.

Acridine dyes, fluorescein and lucifer yellow CH are fluorescent photosensitizers used experimentally to selectively stain and photodynamically destroy eukaryotic cells and subcellular structures. We have determined that the mechanism of light- and oxygen-dependent inactivation of E. coli by these dyes involves oxygen radicals and hydrogen peroxide. All of the dyes oxidized NAD(P)H+ under illumination. Superoxide (O2), detected as the superoxide dismutase (SOD)-inhibitable reduction of ferricytochrome c, was a major product of the dye sensitized photooxidation. Cationic acridine dyes penetrated the membranes of E. coli and were photoreduced intracellularly. Reduced dyes diffused back into the medium and mediated the reduction of extracellular ferricytochrome c. The anionic dyes fluorescein and lucifer yellow CH were unable to mediate extracellular cytochrome c reduction, indicating that these dyes were impermeable to the E. coli membrane. Acridine dyes, when illuminated, inhibited the growth of E. coli in a rich medium, and induced the synthesis of SOD. Fluorescein and lucifer yellow CH did not inhibit growth or induce SOD synthesis because they were unable to enter the cells. Superoxide (O2) and hydrogen peroxide (H2O2), generated by the enzyme xanthine oxidase were toxic to E. coli B. Inactivation by xanthine oxidase was partially inhibited by exogenous SOD and completely inhibited by exogenous catalase or SOD plus catalase. Similarly, exogenous SOD plus catalase protected against inactivation by acridines and fluorescein-NADH or lucifer yellow CH-NADH mixtures. Prior induction of superoxide dismutase and catalase in E. coli B significantly protected cells against a subsequent challenge by illuminated acridine dyes. SOD and catalases preinduction combined with additions of exogenous SOD and catalase completely protected E. coli B against photodynamic inactivation by acridine yellow. The hydroxyl radical scavengers, dimethyl sulfoxide, sodium benzoate and thiourea, protected E. coli B against photodynamic inactivation by acridine orange. The results implicate O2, H2O2, and the hydroxyl radical (OH) as underlying molecular agents of the phototoxicity mediated by acridine orange, acridine yellow, fluorescein and lucifer yellow CH.

Acridine Orange↗

PubMed1995

Spectroscopic studies on the interaction of three partially hydrogenated acridine dyes with calf thymus DNA and their structural comparison.

The interaction of three partially hydrogenated acridine dyes (acridine I, acridine II and acridine III) with calf thymus DNA was studied using spectrophotometric and spectrofluorometric methods. This paper presents the evidence for the formation of complexes between acridine I, II and III with calf thymus DNA. From the results of this studies various binding parameters were evaluated. The binding constant for acridine I and acridine III ranged from 2.1 to 4.4 x 10(5) M-1 for the P/D ratio from 4.29 to 0.56 while for acridine II this constant increased from 0.78 to 2.26 x 10(5) M-1 for the P/D ratio 12 to 2.38 and decreased to 1.47 at P/D ratio 1.34. The Scatchard analysis indicated a cooperative binding of acridine II to calf thymus DNA as compared to acridine I and III. A red shift in the visible absorption bands for dye DNA complexes (for acridine I = 8, acridine II = 7, and acridine III = 9 nm) suggested an electronically coupled interaction mode for the dyes. It is concluded that acridine II interacted stronger with calf thymus DNA than acridine I or III. The results are interpreted in terms of their crystal structures and also with the already reported DNA binder structures.

Acridines↗

PubMed1975

The influence of acridine dyes and caffeine on recovery from ultraviolet damage in Eudorina elegans.

Caffeine and the acridine dyes, acridine orange and acriflavine, were used to examine the repair potential in Eudorina elegans following ultraviolet irradiation. Acridines blocked photoreactivation primarily as a result of absorption of photoreactivating wavelengths, but acridines did not influence dark survival. Therefore, an acridine-sensitive excision-resynthesis-repair process is absent in Eudorina. Caffeine decreased both dark and light survival, the latter only after relatively high doses of ultraviolet light were used for inactivation. The caffeine-sensitive repair process appears to function most actively when the organisms are engaged in DNA synthesis, indicating that a postreplication-repair system exists in Eudorina. However, the data suggest that a repair system not associated with the DNA synthetic phases may also exist.

Acridines↗

PubMed1986

[Competitive interaction of serotonin and the dye acridine orange with DNA].

The interaction of serotonin and acridine orange dye with DNA isolated from bacterium Escherichia coli and the yeast Candida utilis has been analysed by spectrofluorimetric method. Using data on competitive binding to DNA of serotonin and acridine orange, known as DNA intercalator, a conclusion concerning the formation of intercalated complex between serotonin and DNA has been made. It is shown that for yeast DNA the constant of intercalated binding of serotonin is 3,5-fold smaller than for the bacterial one.

Acridine Orange↗

PubMed1981

[Action of acridine dyes on antibiotic, pigment and aerial mycelium formation in streptomycete producers of multicomponent antibiotics].

The ability of 5 streptomycetous species synthesizing multicomponent antibiotic to produce the antibiotic and water-soluble pigment and to form the aerial mycelium in the presence of acridine dyes was studied. It was found that the character of the produced complex changed, when acridine dyes were added to the medium under conditions not affecting the culture growth and the temperature was elevated. Colonies deficient with respect to formation of the aerial mycelium and with changed pigment and antibiotic production were detected in the monospore cultures of the streptomycetes treated with acridine dyes, when the spore survival was equal to 100 percent, the frequency of the colonies being about 40 per cent.

Acridines↗

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↗

PubMed1979

Photodynamic effects of dyes on bacteria. II. Genetic effects of broad-spectrum visible light in the presence of acridine dyes and methylene blue in chemostat cultures of Escherichia coli.

Photodynamic mutagenesis was studied in chemostat cultures of Escherichia coli B/r (TlR trp) exposed to one of six different acridine dyes or methylene blue. Mutation to phage T5 resistance was induced with a broad-spectrum fluorescent-light source. All of the agents tested were photomutagenic; acridine yellow was the most efficient sensitizer and quinacrine was the least efficient. Quinacrine also was moderately mutagenic in the dark, in contrast to the other agents tested, which were not significantly mutagenic in the dark at the low concentrations tested for photomutagenesis. The mutation rate with acridine orange was directly proportional to both fluence rate and dye concentration over the ranges tested. Photomutation rates with acridine orange, proflavine and methylene blue were independent of growth rate of the chemostat cultures. These results are consistent with photomutagenesis occurring as the result of photochemical damage to DNA-dye complexes, independent of cell expression was approximately 2.5 generations for each of the photomutagens tested. This short expression delay supports an earlier segregational model for expression of phage resistance. The following results suggest that photodynamic mutagenesis is due mainly to intercalated dye molecules: (1) both acridine and 9-aminoacridine are photodynamic mutagens; (2) acridine inhibits photomutagenesis with acridine orange; and (3) neither putrescine or spermine, which bind to DNA without intercalating, inhibited photomutagenesis by acridine orange or proflavine.

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↗

PubMed1975

[The effect of actinomycin d, acridine dyes and related substances on the biosynthesis of nucleic acids in normal and leukemic white blood cells. Comparative investigation in intact cells and in a cell-free system (author's transl)].

Acridine dyes inhibit the incorporation of 3H-thymidine and 3H-uridine in intact cells to the same extent as Actinomycin D. In contrast to Actinomycin D, RNA synthesis by DNA - dependent RNA polymerase in a cell-free system is inhibited at lo2 higher concentrations of acridine dyes, only. Possible differential effects on the cell membrane resulting in decreased intracellular pools of uridine and thymidine are discussed.

Acridines↗

PubMed1972

The interaction of acridine dyes with the densely packed DNA of bacteriophage.

The interactions of acridine dyes with intact phage DNA differ from those with extracted DNA in the following respects. Strong binding (intercalation) is greatly reduced in intact phage but probably not eliminated. The cooperative, weak binding is stronger and the stacking tendency is increased. In gels of DNA the stacking tendency is seen to increase with decreasing hydration. These influences of the dense packing of DNA must be taken into account when using basic dyes to study chromosome structure.

Acridines↗

PubMed1992

H+/glycyl-glycine cotransport in eel intestinal brush-border membrane vesicles: studies with the pH-sensitive dye Acridine orange.

Monitoring the fluorescence quenching of the pH-sensitive dye Acridine orange, proton accumulation in the presence of an inside-negative transmembrane potential was measured in eel (Anguilla anguilla) intestinal brush-border membrane vesicles. It was demonstrated that the proton accumulation was specifically increased by the presence of the dipeptide glycyl-glycine in the extravesicular space, showing saturation kinetics at increasing dipeptide concentrations and was specifically inhibited by diethylpyrocarbonate. Data reported suggest the presence of an electrical-potential-dependent H+/glycyl-glycine cotransport system in the eel intestinal brush-border membrane vesicles.

Acridine Orange↗

PubMed1999

The pH-sensitive dye acridine orange as a tool to monitor exocytosis/endocytosis in synaptosomes.

We introduce the use of the pH-sensitive dye acridine orange (AO) to monitor exo/endocytosis of acidic neurotransmitter-containing vesicles in synaptosomes. AO is accumulated exclusively in acidic v-ATPase-dependent bafilomycin (Baf)-sensitive compartments. A fraction of the accumulated AO is rapidly released (fluorescence increase) upon depolarization with KCl in the presence of Ca2+. The release (completed in 5-6 s) is followed by reuptake to values below the predepolarization baseline. The reuptake, but not the release, is inhibited by Baf added 5 s prior to KCl. In a similar protocol, Baf does not affect the initial fast phase of glutamate release measured enzymatically, but it abolishes the subsequent slow phase. Thus, the fast AO release corresponds to the rapid phase of glutamate release and the slow phase depends on vesicle cycling. AO reuptake depends in part on the progressive accumulation of acid-loaded vesicles during cycling. Stopping exocytosis at selected times after KCl by Ca2+ removal with EGTA evidences endocytosis: Its T(1/2) was 12 +/- 0.6 s. The K(A)+, channel inhibitors 4-aminopyridine (100 microM) and alpha-dendrotoxin (10-100 nM) are known to induce glutamate release by inducing the firing of Na+ channels; their action is potentiated by the activation of protein kinase C. Also these agents promote a Ca2+-dependent AO release, which is prevented by the Na+ channel inhibitor tetrodotoxin and potentiated by 4beta-phorbol 12-myristate 13-acetate (PMA). With alpha-dendrotoxin, endocytosis was monitored by stopping exocytosis at selected times with EGTA or alternatively with Cd2+ or tetrodotoxin. The T(1/2) of endocytosis, which was unaffected by PMA, was 12 +/- 0.4 s with EGTA and Cd2+ and 9.5 +/- 0.5 s with tetrodotoxin. Protein kinase C activation appeared to facilitate vesicle turnover.

4-Aminopyridine↗

PubMed1981

Acridine dyes and other DNA-intercalating agents induce the luminescence system of luminous bacteria and their dark variants.

Acridine dyes and other DNA-intercalating agents such as ethidium bromide, theophylline, and caffeine induce luminescence in dark variants (K variants) different luminous species of bacteria, as well as in their wild-type luminous cells, prior to induction. The increase in luminescence appears 10-20 min after addition of these agents and is inhibited by chloramphenicol or rifampicin. Addition of these agents affects the synthesis of both luciferase and aldehyde-synthesizing enzymes. It is hypothesized that these agents, through their intercalation into DNA, cause configurational changes resulting in derepressed transcription of the luminescence operon.

Acridines↗

PubMed1982

[Effect of acridine dyes on the ultrastructure of mitochondria in HeLa and LM cells].

Fluorescent staining of mitochondria in living HeLa cells and mouse fibroblasts (LM) with acridine dyes has been reported recently. The investigations are now extended to electron microscopy. Dyes used in our vital staining experiments are 10-ethyl- and 10-(2-iodethyl)acridine orange hydrochloride (EAO, IAO). The mitochondria of vitally stained cells are compared with untreated material. There are dramatic changes of the ultrastructure of HeLa mitochondria within the short incubation time of a few minutes. During the same time only small alterations of LM mitochondria could be observed.

Acridine Orange↗

PubMed1972

Use of uncoupling acridine dyes as stoichiometric energy probes in chloroplasts.

In a suspension of spinach chloroplasts the fluorescence of atebrin and other uncoupling acridine dyes is quenched upon energization which is associated with a proportional binding of the dyes to the organelles. There is a stoichiometric relation between the amount of dye bound and the actual steady state level of energy. When the concentration of atebrin is increased in energized chloroplasts the fluorescence is completely quenched until a certain concentration is attained above which the response sharply declines. Such titrations with atebrin were carried out under conditions of partial electron transport governed by photosystems I and II, in the presence of 3-(3,4-dichlorophenyl)-1, 1-dimethylurea and cyanide, respectively, and of complete electron transport governed by the two photo-systems. The sum of the saturating amounts of atebrin obtained in these partial electron flow systems equals that obtained in the complete system. This lends strong support to the view that two sites of energy conservation are coupled to the linear photosynthetic electron transport.When ATP was the energy donor the saturating amounts of atebrin were the same in both control and cyanide-treated chloroplasts, indicating that the energy-conserving mechanism was unimpaired in the latter.Removal of the chloroplast-coupling factor by ethylenedia-minetetraacetate treatment leads to inhibition of the probe responses, which can be restored again in recoupled chloroplasts.

Journal Article↗

PubMed1969

Mechanisms of inhibition of pyrimidine dimer formation in deoxyribonucleic acid by acridine dyes.

The ultraviolet (UV)-induced formation of cyclobutyl pyrimidine dimers in Escherichia coli deoxyribonucleic acid (DNA) in vitro has been investigated in terms of the mechanism of inhibition by acridine dyes, the effect on dimer yield of specific singlet and triplet quenchers, and the mechanism of dimer formation. Our results indicate that (a) energy transfer is important in dimer reduction by acridines, (b) this transfer occurs from the singlet (S(1)) of DNA, and (c) at room temperature triplet quenchers do not reduce dimer yield in DNA.

Acetone↗