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PubMed2005

Purification and characterization of polyphenol oxidase from nettle (Urtica dioica L.) and inhibitory effects of some chemicals on enzyme activity.

Polyphenol oxidase (PPO) of nettle (Urtica dioica L.) was extracted and purified through (NH4)2SO4 precipitation, dialysis, and CM-Sephadex ion-exchange chromatography and was used for its characterization. The PPO showed activity to catechol, 4-methylcatechol, L-3,4-dihydroxyphenylalanine (L-DOPA), L-tyrosine, p-cresol, pyrogallol, catechin and trans-cinnamic acid. For each of these eight substrates, optimum conditions such as pH and temperature were determined and L-tyrosine was found to be one of the most suitable substrates. Optimum pH and temperature were found at pH 4.5 and 30 degrees C respectively and Km and Vmax values were 7.90 x 10(-4) M, and 11290 EU/mL for with L-tyrosine as substrate. The inhibitory effect of several inhibitors, L-cysteine chloride, sodium azide, sodium cyanide, benzoic acid, salicylic acid, L-ascorbic acid, glutathione, thiourea, sodium diethyl dithiocarbamate, beta-mercaptoethanol and sodium metabisulfite were tested. The most effective was found to be sodium diethyl dithiocarbamate which acted as a competitive inhibitor with a Ki value of 1.79 x 10(-9)M. In addition one isoenzyme of PPO was detected by native polacrylamide slab gel electrophoresis.

Ascorbic Acid↗
PubMed1958

Metabolic factors and ventricular fibrillation.

Ventricular fibrillation has been studied in the isolated rabbit heart to determine the effect of factors modifying the metabolism. Sodium azide, sodium monoiodoacetate and sodium fluoride were found to cause fibrillation, the effect of sodium fluoride being neutralized by magnesium chloride. Fibrillation was also caused by lack of glucose and could be arrested by adding glucose; the effect of glucose in arresting fibrillation was facilitated by insulin. In other experiments mannose and pyruvate could arrest fibrillation due to lack of glucose, but L(-)lactate could not. The effect of temperature changes, of adrenaline and of cyanide were also studied. When all oxygen was removed from the perfusing solution fibrillation was arrested.

Arrhythmias, Cardiac↗
PubMed1990

Neutrophil-mediated cytotoxicity induced by secretory IgA.

Normal human neutrophils triggered by secretory IgA (sIgA) displayed low levels of cytotoxicity towards non-sensitized red blood cells. Catalase completely impaired this non-specific cytotoxicity (NSC), while superoxide dismutase (SOD) significantly enhanced it, suggesting a key role for hydrogen peroxide (H2O2) in the lysis of target cells. Three heme-enzyme inhibitors, sodium azide, sodium cyanide and 3-amino-1,2,4-triazole, did not decrease NSC, but significantly enhanced it, suggesting that the mechanism involved is not dependent upon myeloperoxidase (MPO). Heat-aggregated IgG (HA-IgG) synergize with sIgA in promoting NSC. It was also found that gamma interferon significantly enhanced neutrophil-mediated NSC induced by sIgA, its effect being more dramatic on NSC triggered by low concentrations of sIgA. The significance of these results is discussed.

Amitrole↗
PubMed1984

Active transport of lead-210 by everted segments of rat duodenum.

Everted gut sacs prepared from rat duodenum can transfer 210Pb from mucosal to serosal surfaces against concentration gradients in vitro. The mechanism requires oxygen and is significantly inhibited by sodium azide, sodium iodoacetate, 2,4-dinitrophenol, sodium cyanide, and sodium fluoride. Lack of oxygen or the presence of metabolic inhibitors produced greater relative inhibition of net serosal transfer but greater absolute decrements of net mucosal uptake. Treatment of rats prior to sac preparation with either intravenous FeCl2 or endotoxin, or the addition of FeCl2 to the mucosal medium, selectively inhibited net serosal transfer. Net mucosal uptake and net serosal transfer were significantly negatively correlated with animal weight. Jejunal or ileal sacs did not actively transport 210Pb.

2,4-Dinitrophenol↗
PubMedDate not supplied

Specific features of the electroretinogram of vertebrates induced by X-rays.

The net electroretinograms of dark-adapted retinas of the common frog in situ were investigated on an automated experimental system with programmed control and electronic differentiation of biopotentials with respect to the first and second derivatives. It was demonstrated that X-rays elicit an electroretinogram consisting of two components, provisionally called the first and second X-ray reactions (X-1 and X-2), which differ with respect to their parameters from electroretinograms elicited under the same conditions by red and blue light. The administration of sodium azide, sodium nitrate, monoiodo-acetate and other substances alter the X-1 and X-2 as well as the photo-induced ERGs in different ways; this indicates their relative independence and different mechanisms of the occurrence and passing of excitation across the structures of the retina, and makes it possible to partially isolate these for individual study. Thus, the assertion of a number of investigators regarding the absence of specific features in the X-ray induced electroretinograms becomes problematical. The discovery of X-ray-specific reactions in the retina makes it possible to hope that the radiological phosphene (the X-ray phosphene) may serve as a test for the determination of the individual radiational excitability of the central nervous system.

Animals↗
PubMed1981

Carcinogenicity tests of certain environmental and industrial chemicals.

Fourteen chemicals of varied uses were tested for carcinogenicity by oral administration in male and female Charles River CD rats. Under the conditions of the tests, propane sultone, propylene imine, and ethylenethiourea, in addition to the positive control N-2-fluorenylacetamide, were carcinogenic. Avadex, bis(2-chloroethyl) ether, the potassium salt of bis(2-hydroxyethyl) dithiocarbamic acid, ethylene carbonate, and semicarbazide hydrochloride were not carcinogenic under the test conditions. Dithiooxamide, glycerol alpha-monochlorohydrin, and thiosemicarbazide gave somewhat ambiguous results, though administered at high enough dose levels to be toxic. An inadequate number of animals survived treatments with sodium azide, sodium bisulfide, and vinylene carbonate, or the animals may not have received sufficiently high doses of the test chemicals to provide maximum test sensitivity. However, there were no indications that these three chemicals were carcinogenic under the test conditions.

2-Acetylaminofluorene↗
PubMed1973

Stereospecific binding of the potent narcotic analgesic (3H) Etorphine to rat-brain homogenate.

Etorphine, the most potent narcotic analgesic known, was labeled with tritium by catalytic exchange. This drug exhibits stereospecific, saturable binding to rat-brain homogenate. At saturation, the stereospecific binding is 0.1-0.15 pmol/mg of protein. Specific binding is inhibited high salt concentrations, sulfhydryl reagents, and proteolytic enzymes, but is unaffected by phospholipases A and C, sodium azide, sodium fluoride, and prostaglandins E(1) and E(2). Competition for binding of [(3)H]etorphine correlates with agonist and antagonist potencies. The stable, stereospecific binding of an active narcotic analgesic supports the existence of opiate receptors.

Acetamides↗
PubMed1974

Active transport of alcohol in Corynebacterium acetophilum.

The transport of alcohols was studied in Corynebacterium acetophilum, which was isolated as a strain growing well on acetate and ethanol. The transport of ethanol was found to be inducible by ethanol, n-propanol, n-butanol, and acetate, whereas transport of methanol occurred by noninducible passive diffusion. The entry of ethanol into the cells occurred against a concentration gradient and showed saturation kinetics with two K(m) values of 2.4 x 10(-5) M and 6.0 x 10(-5) M. Uptake of ethanol was inhibited by sodium azide, sodium cyanide, 2,4-dinitrophenol, and p-chloromercuribenzoate. The transport of ethanol was competitively inhibited by normal alcohols, but not by iso- or tert-alcohols. From these studies, we concluded that an inducible active alcohol transport system mediates the entry of ethanol, n-propanol, or n-butanol into the cells of C. acetophilum.

1-Propanol↗
PubMed1977

Nitric oxide activates guanylate cyclase and increases guanosine 3':5'-cyclic monophosphate levels in various tissue preparations.

Nitric oxide gas (NO) increased guanylate cyclase [GTP pyrophosphate-lyase (cyclizing), EC 4.6.1.2] activity in soluble and particulate preparations from various tissues. The effect was dose-dependent and was observed with all tissue preparations examined. The extent of activation was variable among different tissue preparations and was greatest (19- to 33-fold) with supernatant fractions of homogenates from liver, lung, tracheal smooth muscle, heart, kidney, cerebral cortex, and cerebellum. Smaller effects (5- to 14-fold) were observed with supernatant fractions from skeletal muscle, spleen, intestinal muscle, adrenal, and epididymal fat. Activation was also observed with partially purified preparations of guanylate cyclase. Activation of rat liver supernatant preparations was augmented slightly with reducing agents, decreased with some oxidizing agents, and greater in a nitrogen than in an oxygen atmosphere. After activation with NO, guanylate cyclase activity decreased with a half-life of 3-4 at 4 degrees but re-exposure to NO resulted in reactivation of preparations. Sodium azide, sodium nitrite, hydroxylamine, and sodium nitroprusside also increased guanylate cyclase activity as reported previously. NO alone and in combination with these agents produced approximately the same degree of maximal activation, suggesting that all of these agents act through a similar mechanism. NO also increased the accumulation of cyclic GMP but not cyclic AMP in incubations of minces from various rat tissues. We propose that various nitro compounds and those capable of forming NO in incubations activate guanylate cyclase through a similar but undefined mechanism. These effects may explain the high activities of guanylate cyclase in certain tissues (e.g., lung and intestinal mucosa) that are exposed to environmental nitro compounds.

Animals↗
PubMed1975

Potassium fluxes in Neocosmospora vasinfecta.

The unidirectional K+ fluxes across the mycelial surface of Neocosmospora vasinfecta were determined using 42K. Influx was mediated by at least two kinetically distinct systems, one having an apparent Km of 6-5 mu-equiv. K+/l and the other of about 1-0 m-equiv. K+/l. The VMAX for both systems was in the range 18 to 22 mu-equiv. K+/100 mg mycelial dry matter/h (1-0 to 1-2 m-equiv. K+/l cell-water/min). Influx was strongly inhibited by 2,4-dinitrophenol, sodium azide, sodium arsenate and anaerobiosis. K+ efflux was dependent on the external K+ concentration and ranged from 3 to 10% of mycelial K+/h. The maximum efflux rate was always considerably less than the initial influx rate for the K+ concentrations examined. During incubation in dilute KCl solutions, K+ influx decreased to a value approaching the K+ efflux rate. It is considered that equilibrium with external K+ is attained primarily by the regulation of K+ influx, and that this may be the principal mechanism controlling cytoplasmic K+ levels. Adsorption of K+ was also observed throughout the K+ concentration range examined and can be attributed to two distinct K+-binding entities at the mycelial surface, half-saturating at approximately O-I mM-and 4-4 mM-KCl respectively.

Adsorption↗
PubMed1993

Phosphorylated nutrient uptake by Treponema denticola and other potential periodontopathogens.

Nutrient uptake may contribute to the survival of certain potential periodontopathogens in the competitive environment of the gingival sulcus. This study was conducted to assess the uptake of commercially available, key radiolabelled phosphorylated compounds by Treponema denticola. There was a linear relationship in the uptake of ATP and G-1-P with cell concentrations of 0.1-2.5 mg of cell dry weight. This uptake reached a steady state within 15 min, and at temperatures of 25-37 degrees C the uptake ranged between 13-21%. At 50 degrees C, or above 50 degrees C the assay cells took up 0-1% of the assay nutrients. The maximum uptake of ATP was 47.5, 38 and 47.6 pmoles for serovars a, b and c. G-1-P yielded maximum uptake values of 306, 304, and 306 pmoles respectively. Significant uptake of ATP, or G-1-P occurred at pH 4.8 for serovars a, or c, while serovar b showed a broad pH range for the uptake of G-1-P. Stannous fluoride at a concentration of 0.17 mM enhanced the uptake of ATP while chlorhexidine digluconate inhibited the uptake of ATP. At concentrations usually employed (0.05-0.5 mM) the metabolic poisons 2,4-dinitrophenol, sodium azide, sodium arsenite and the ATPase inhibitor N,N1-dicyclohexylcarbodiimide did not alter significantly the uptake of ATP. The uptake of ATP, by Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, Fusobacterium nucleatum and T. denticola at pH 4.8 was 13.4, 1.5, 6.9, and 18-20.4%, respectively. At pH 6.5 the uptake for the microorganisms indicated above was 22, 1.3, 6.6 and 6.2%, respectively. G-1-P showed the same trend in its uptake by A. actinomycetemcomitans, P. gingivalis, F. nucleatum and T. denticola. This study provides for the first time specific examples of phosphorylated nutrient uptake by potential periodontopathogens, and that the uptake of phosphorylated nutrients can be suppressed by oral hygienic compounds.

Adenosine Triphosphate↗
PubMed1993

Chemiluminescence in activated human neutrophils: role of buffers and scavengers.

Human neutrophils (PMNs) suspended in Hanks' balanced salt solution (HBSS), which are stimulated either by polycation-opsonized streptococci or by phorbol myristate acetate (PMA), generate nonamplified (CL), luminol-dependent (LDCL), and lucigenin-dependent chemiluminescence (LUCDCL). Treatment of activated PMNs with azide yielded a very intense CL response, but only a small LDCL or LUCDCL responses, when horse radish peroxidase (HRP) was added. Both CL and LDCL depend on the generation of superoxide and on myeloperoxidase (MPO). Treatment of PMNs with azide followed either by dimethylthiourea (DMTU), deferoxamine, EDTA, or detapac generated very little CL upon addition of HRP, suggesting that CL is the result of the interaction among H2O2, a peroxidase, and trace metals. In a cell-free system practically no CL was generated when H2O2 was mixed with HRP in distilled water (DW). On the other hand significant CL was generated when either HBSS or RPMI media was employed. In both cases CL was markedly depressed either by deferoxamine or by EDTA, suggesting that these media might be contaminated by trace metals, which catalyzed a Fenton-driven reaction. Both HEPES and Tris buffers, when added to DW, failed to support significant HRP-induced CL. Nitrilotriacetate (NTA) chelates of Mn2+, Fe2+, Cu2+, and Co2+ very markedly enhanced CL induced by mixtures of H2O2 and HRP when distilled water was the supporting medium. Both HEPES and Tris buffer when added to DW strongly quenced NTA-metal-catalyzed CL. None of the NTA-metal chelates could boost CL generation by activated PMNs, because the salts in HBSS and RPMI interfered with the activity of the added metals. CL and LDCL of activated PMNs was enhanced by aminotriazole, but strongly inhibited by diphenylene iodonium (an inhibitor of NADPH oxidase) by azide, sodium cyanide (CN), cimetidine, histidine, benzoate, DMTU and moderately by superoxide dismutase (SOD) and by deferoxamine LUCDCL was markedly inhibited only by SOD but was boosted by CN. Taken together, it is suggested that CL generated by stimulated PMNs might be the result of the interactions among, NADPH oxidase, (inhibitable by diphenylene iodonium), MPO (inhibitable by sodium azide), H2O2 probably of intracellular origin (inhibitable by DMTU but not by catalase), and trace metals that contaminate salt solutions. The nature of the salt solutions employed to measure CL in activated PMNs is critical.

Acridines↗
PubMed1993

DNA cleavage by metabolites of butylated hydroxytoluene.

The effect of butylated hydroxytoluene (BHT) and its metabolites on DNA cleavage in vitro was studied with supercoiled plasmid DNA, pUC18, by agarose gel electrophoresis. Among several BHT metabolites, 2,6-di-t-butyl-p-benzoquinone (BHT-quinone) caused cleavage of supercoiled DNA (form I) at a concentration as low as 1 x 10(-6) M. The relative amount of linear form (form III) was increased with increasing concentration of BHT-quinone. 2,6-Di-t-butyl-4-hydroperoxy-4-methyl-2,5-cyclohexadienone (BHT-peroxyquinol) and 3,5-di-t-butyl-4-hydroxybenzaldehyde (BHT-CHO) also cleaved DNA, but to a lesser extent than BHT-quinone. No DNA cleavage was detected by BHT, 2,6-di-t-butyl-4-hydroxymethyl phenol (BHT-OH), 3,5-di-t-butyl-4-hydroxybenzoic acid (BHT-COOH), 2,6-di-t-butyl-4-hydroxy-4-methyl-2,5-cyclohexadienone (BHT-quinol) or 2,6-di-t-butyl-4-methylene-2,5-cyclohexadienone (BHT-quinone methide). The DNA cleavage by BHT-quinone was inhibited by oxygen radical scavengers including superoxide dismutase (SOD), catalase, polyethylene glycol, t-butyl alcohol, dimethyl sulfoxide, sodium azide, sodium benzoate, bovine serum albumin and methionine, while it was enhanced by the addition of FeCl2. The production of superoxide radical in a solution of BHT-quinone was confirmed by cytochrome c reduction assay. Superoxide was not produced by BHT or other BHT metabolites except for BHT-quinone. These results suggest that BHT-quinone, one of the principal metabolites of BHT, cleaves DNA strands via its generation of oxygen radicals.(ABSTRACT TRUNCATED AT 250 WORDS)

Butylated Hydroxytoluene↗
PubMed1990

DNA cleavage by phenylhydroquinone: the major metabolite of a fungicide o-phenylphenol.

The interaction of o-phenylphenol (OPP) and its metabolites with DNA was examined. As a model system, the reactivities of OPP and its metabolites with DNA were studied by using pUC18 DNA. The major metabolite formed in vitro from OPP by mixed function oxidase was phenylhydroquinone (PHQ). This result corresponds to the findings that PHQ in the form of glucuronide conjugate was the main product detected in bladder of OPP fed rats in vivo. When supercoiled pUC18 DNA (form I) was incubated with PHQ at concentrations from 1 X 10(-6) M to 2 X 10(-1) M, DNA strand scission by PHQ was observed at a concentration as low as 1 X 10(-5) M and the amount of linear form (form III) increased with increasing PHQ concentration. PHQ causes DNA strand scission. The DNA cleavage by OPP and phenyl-p-benzoquinone (PBQ) was barely detectable. The DNA cleavage by PHQ was inhibited by superoxide dismutase (SOD), catalase and several oxygen radical scavengers such as polyethylene glycol, tert-butanol, dimethyl sulfoxide, sodium azide, sodium benzoate, bovine serum albumin and methionine. The production of superoxide radical from PHQ was confirmed by cytochrome c reduction assay. These results indicate that the oxygen radicals such as superoxide, hydroxyl radicals and some others generated in the process of oxidation of PHQ in aqueous solution are responsible for the DNA cleavage. In order to identify the sites of cleavage of DNA by PHQ, a 5'-end 32P-labeled 206 base-pair EcoRI-BglI fragment of pUC18 DNA was incubated with PHQ. The DNA was then analyzed by sequencing gel electrophoresis followed by autoradiography. When the DNA was incubated with PHQ and further treated with piperidine, cleavage was detected relatively more frequently at guanine residues. The attack seemed to occur at guanine residues in general, but was not restricted to guanines with specific residues in the vicinity.

Animals↗
PubMed1979

Synthesis of adenosine 3',5'-monophosphate by guanylate cyclase, a new pathway for its formation.

The 105 000 X g gupernatant fractions from homogenates of various rat tissues catalyzed the formation of both cyclic GMP and cyclic AMP from GTP and ATP, respectively. Generally cyclic AMP formation with crude or purified preparations of soluble guanylate cyclase was only observed when enzyme activity was increased with sodium azide, sodium nitroprusside, N-methyl-N'-nitro-N-nitrosoguanidine, sodium nitrite, nitric oxide gas, hydroxyl radical and sodium arachidonate. Sodium fluoride did not alter the formation of either cyclic nucleotide. After chromatography of supernatant preparations on Sephadex G-200 columns or polyacrylamide gel electrophoresis, the formation of cyclic AMP and cyclic GMP was catalyzed by similar fractions. These studies indicate that the properties of guanylate cyclase are altered with activation. Since the synthesis of cyclic AMP and cyclic GMP reported in this study appears to be catalyzed by the same protein, one of the properties of activated guanylate cyclase is its ability to catalyze the formation of cyclic AMP from ATP. The properties of this newly described pathway for cyclic AMP formation are quite different from those previously described for adenylate cyclase preparations. The physiological significance of this pathway for cyclic AMP formation is not known. However, these studies suggest that the effects of some agents and processes to increase cyclic AMP accumulation in tissue could result from the activation of either adenylate cyclase or guanylate cyclase.

Animals↗
PubMed1991

Effects of copper and tributyltin on stress protein abundance in the rotifer Brachionus plicatilis.

1. Exposure of the rotifer Brachionus plicatilis to elevated temperature resulted in the synthesis of a number of proteins, including a prominent one of 58,000 Da (SP58). 2. This protein is immunologically crossreactive with the 65,000 Da heat shock protein of the moth Heliothis virescens, which is a member of a highly conserved family of mitochondrial proteins. 3. Exposure of rotifers to sublethal doses of CuSO4 leads to a 4-5-fold increase in abundance of SP58, with maximum increase occurring at a dose that is approximately 5% of the LC50 for that compound. 4. A similar response was seen with tributyl tin (TBT). Kinetics of induction were sigmoidal, with induction occurring in the range of 20-30 micrograms/l. 5. No response was observed when rotifers were exposed to aluminum chloride, mercury chloride, pentachlorophenol, sodium arsenite, sodium azide, sodium dodecyl sulfate, or zinc chloride. 6. These results indicate that changes in stress protein abundance may prove useful as a biomarker of exposure to particular toxicants.

Animals↗
PubMedDate not supplied

Partial characterization of guanylate cyclase activity of the human placenta.

An optimal assay system for the measurement of GC activity in subcellular fractions of human placenta homogenates was developed. MN2+ was more effective than Mg2+ as a cofactor and, in addition, it markedly potentiated the Mg2+-dependent GC activity. The apparent optimal temperature for GC activity was 45 degrees C and the pH optimum was in the range of 7.5 to 8.3. The apparent Km of Mn2+-dependent GC for GTP was 0.1 and that of MG2+-dependent GC for GTP was 0.4 mm. More than 95 per cent of GC activity was associated with the 100 000 X g supernatant fraction. ATP at a concentration of 0.5 mm inhibited GC activity by 50 per cent. The Mn2+-dependent GC activity was inhibited by p-hydroxymercuriphenyl sulphonate at concentrations between 10 and 50 micrometers; this inhibition was reversed, in part, by dithiothreitol at concentrations of 150 to 500 micrometers to approximately one-fifth the activity of control values. In addition, we found that dithiothreitol was an inhibitor of GC activity. Studies on the responsiveness of placental GC to nucleophilic compounds indicated that phenylhydrazine was the most potent stimulus, while hydroxylamine, hydrazine, sodium azide, sodium nitrite and sodium nitroprusside were less potent. Placental GC was unaffected by alpha- and beta-adrenergic agonists or by cholinergic agonist, as well as by steroids produced by the placenta.

Cyclic GMP↗
PubMed2005

Tunable DNA photocleavage by an acridine-imidazole conjugate.

We report the synthesis and characterization of photonucleases N,N'-bis[2-[bis(1H-imidazol-4-ylmethyl)amino]ethyl]-3,6-acridinediamine (7) and N-[2-[bis(1H-imidazol-4-ylmethyl)amino]ethyl]-3,6-acridinediamine (10), consisting of a central 3,6-acridinediamine chromophore attached to 4 and 2 metal-coordinating imidazole rings, respectively. In DNA reactions employing 16 metal salts, photocleavage of pUC19 plasmid is markedly enhanced when compound 7 is irradiated in the presence of either Hg(II), Fe(III), Cd(II), Zn(II), V(V), or Pb(II) (low-intensity visible light, pH 7.0, 22 degrees C, 8-50 microM 7). We also show that DNA photocleavage by 7 can be modulated by modifying buffer type and pH. Evidence of metal complex formation is provided by EDTA experiments and by NMR and electrospray ionization mass spectral data. Sodium azide, sodium benzoate, superoxide dismutase, and catalase indicate the involvement of type I and II photochemical processes in the metal-assisted DNA photocleavage reactions. Thermal melting studies show that compound 7 increases the Tm of calf thymus DNA by 10 +/- 1 degrees C at pH 7.0 and that the Tm is further increased upon the addition of either Hg(II), Cd(II), Zn(II), or Pb(II). In the case of Fe(III) and V(V), a colorimetric assay demonstrates that compound 7 sensitizes one electron photoreduction of these metals to Fe(II) and V(IV), likely accelerating the production of type I reactive oxygen species. Our data collectively indicate that buffer, pH, Hg(II), Fe(III), Cd(II), Zn(II), V(V), Pb(II), and light can be used to "tune" DNA cleavage by compound 7 under physiologically relevant conditions. The 3,6-acridinediamine acridine orange has demonstrated great promise for use as a photosensitizer in photodynamic therapy. In view of the distribution of iron in living cells, compound 7 and other metal-binding acridine-based photonucleases should be expected to demonstrate excellent photodynamic action in vivo.

Aminoacridines↗