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At least 19 recordsLinked to original sources
PubMed1998

Association of 6- and 8-Hydroxyquinolines with Aerosol-OT in Heptane: Competition with Dimerization of 8-Hydroxyquinoline.

The enhancement and shift of the fluorescence spectrum of 8-hydroxyquinoline (8-HQ) in heptane upon gradual additions of the anionic surfactant aerosol-OT (AOT) allowed us to show that monomeric 8-HQ was progressively associated to the polar heads via H-bonding. This association competes with dimerization of 8-HQ in heptane which has been revealed by us in a previous work using vapor pressure osmometry measurements. Similar competition has been qualitatively reported by others in the case of 7-azaindole. In the present work, a comparison between the behaviors of 8- and 6-hydroxyquinoline was undertaken because the positions of the -OH and >/=N functions preclude dimerization in 6-hydroxyquinoline. This comparison resulted in the determinations of the binding constant of 8-HQ to AOT, Kass = 860 +/- 30, and of the dimerization constant in heptane, Kdim = (7.0 +/- 1.5) x 10(7). Hence the dimers of 8-HQ in heptane, never reported before, turned out to be of outstanding stability. Copyright 1998 Academic Press.

Journal Article↗
PubMed2004

Antileishmanial activity of a new 8-hydroxyquinoline derivative designed 7-[5'-(3'-phenylisoxazolino)methyl]-8-hydroxyquinoline: preliminary study.

7-[5'-(3'-phenylisoxazolino)methyl]-8-hydroxyquinoline a new synthetic 8-hydroxyquinoline derivative, was found, for the first time, to inhibit the multiplication in vitro of Leishmania tropica, Leishmania major and Leishmania infantum at micromolar concentrations. For each test we calculated a 50% inhibitory concentration (IC50) and the IC50 values found after 48 h are: 0.4 microgram/ml for L. tropica, 0.88 microgram/ml for L. major and 0.62 microgram/ml for L. infantum. As positive control, amphotericin B, a standard antileishmanial drug was used.

Amphotericin B↗
PubMed1983

[Oral provocation of a hydroxyquinoline eczema. Hematogenic contact eczema from hydroxyquinoline].

We inform about an eczema reaction from inside after perception of Reasec Plus. This hydroxyquinolin substance caused a generalized dermatitis at a patient who is contact sensibilized against Vioform. The sensitivity index found out among our patients is very little (0,85%). The probability for the appearance of an internally or externally induced contact dermatitis after perception of Hydroxyquinolin is rather poor.

Administration, Oral↗
PubMed2006

Electrogenerated chemiluminescence of the lithium salts of 8-hydroxyquinoline and 2-methyl-8-hydroxyquinoline.

The spectroscopy, electrochemistry, and electrogenerated chemiluminescence (ECL) of [(q)(qH)Li]x (qH=8-hydroxyquinolinato) and [(Meq)(MeqH)Li]x (MeQH=2-methyl-8-hydroxyquinolinato) have been investigated. In both acetonitrile and aqueous solutions, [(q)(qH)Li]x and [(Meq)(MeqH)Li]x have absorption maxima at 320 and 309 nm, respectively. When excited at these wavelengths, the complexes emit around 500 nm (blue-green) in acetonitrile. Photoluminescence efficiencies (phiem) were 0.036 for [(q)(qH)Li]x and 0.012 for [(Meq)(MeqH)Li]x when compared to Ru(bpy)3(2+) (bpy=2,2'-bipyridine) with phiem=0.042. No photoluminescence was observed in aqueous media. The complexes show irreversible oxidative electrochemistry and quasi-reversible reductions in acetonitrile. ECL efficiencies (phiecl) were 0.097 for [(q)(qH)Li]x and 0.080 for [(Meq)(MeqH)Li]x when compared to Ru(bpy)(3)2+ (phiecl=1) in aqueous buffered solution and 0.035 for [(q)(qH)Li]x and 0.028 for [(Meq)(MeqH)Li]x in acetonitrile (0.05 M tri-n-propylamine (TPrA) as an oxidative-reductive ECL co-reactant). The ECL peaks at a potential corresponding to oxidation of both the TPrA and [(q)(qH)Li]x or [(Meq)(MeqH)Li]x. Also, qualitative studies using transmission filters suggest that both complexes emit ECL in approximately the same blue-green region as their photoluminescence, indicating that the same excited state is formed in both experiments.

Journal Article↗
PubMed1999

Synthesis and cytotoxicity evaluation of some 8-hydroxyquinoline derivatives.

Interest in Mannich bases of 8-hydroxyquinoline stems from reports of their high potency against human cancer cells. In the search for potential anticancer drug candidates, Mannich bases of 8-hydroxyquinoline (7-pyrrolidinomethyl-8-hydroxyquinoline, 7-morpholinomethyl-8-hydroxyquinoline, 7-piperidinomethyl-8-hydroxyquinoline and 7-diethylaminomethyl-8-hydroxyquinoline) were synthesised by reaction with various secondary amines and formaldehyde. They were prepared as hydrochlorides. The cytotoxic activity of 7-pyrrolidinomethyl-8-hydroxyquinoline, 7-morpholinomethyl-8-hydroxyquinoline and 7-diethylaminomethyl-8-hydroxyquinoline compounds in the National Cancer Institute in-vitro cancer cell line panel was determined. It was found that they exhibited substantial cytotoxic activity against leukaemia. The log concentration of 7-pyrrolidinomethyl-8-hydroxyquinoline, 7-morpholinomethyl-8-hydroxyquinoline and 7-diethylaminomethyl-8-hydroxyquinoline that inhibited 50% of 60 cell lines' growth were -4.81 M, -5.09 M and -5.35 M, respectively. Compound 7-pyrrolidinomethyl-8-hydroxyquinoline was selected for further in-vivo testing. The electrophysiological effect of 7-pyrrolidinomethyl-8-hydroxyquinoline also was tested in human myeloma cells (RPMI 8226). The outward current was voltage dependent, activating at -40 mV and believed to be the voltage-activated K+ current I(K(V)). 7-Pyrrolidinomethyl-8-hydroxyquinoline (1-30 microM) caused the inhibition of I(K(V)) in a concentration-dependent manner. The IC50 value of 7-pyrrolidinomethyl-8-hydroxyquinoline-induced inhibition of I(K(V)) is 23 microM. The GI50 value of 7-pyrrolidinomethyl-8-hydroxyquinoline-induced inhibition of cell growth is 14 microM. The results suggest that at least part of the cytotoxicity effect of 7-pyrrolidinomethyl-8-hydroxyquinoline on myeloma cells could be related to blockade of voltage-activated K+ channels.

Antineoplastic Agents↗
PubMed2006

The evaluation of liposome-water partitioning of 8-hydroxyquinolines and their copper complexes.

Bioavailability and toxicity of mixtures are urgent research issues, but usually mixtures of exclusively organic chemicals or exclusively metals are investigated. In our study, we explored the role of combinations of hydrophobic ionogenic organic compounds (HIOCs) with copper (Cu2+)for uptake and bioavailability of metals and hydrophobic metal complexes in an in vitro membrane system. We investigated the influence of the interactions of copper and 8-hydroxyquinolines, both components used in formulations of pesticides, on their partitioning into liposomes, which are model systems for biological membranes and are composed of lipid bilayers made of phosphatidylcholine. The test set of compounds comprised the parent compound 8-hydroxyquinoline and 8-hydroxyquinolines with hydrophobic (e.g., 5-chloro-8-hydroxyquinoline, 5,7-dichloro-8-hydroxyquinoline, 5,7-dibromo-8-hydroxyquinoline) and with hydrophilic (e.g., 8-hydroxyquinoline-5-sulfonic acid) substituents. Hydrophobic 8-hydroxyquinolines facilitate the passive uptake of copper into phospholipid bilayers by complex formation. Not only the neutral species of the ligands and their neutral copper ligand complexes are significantly taken up into the membrane, but also the cationic and anionic species of the ligands and the cationic complexes. The neutral, anionic, and cationic species of 8-hydroxyquinoline and the hydrophobic substituted 8-hydroxyquinolines exhibit linear correlations between their logarithmic liposome-water partitioning coefficients (log Klipw) and the logarithmic octanol-water partitioning coefficients of their neutral species (log Kow, neutral). The neutral species show the strongest partitioning followed by the anionic and cationic species. The associated quantitative structure activity relationships describing the dependency of log Klipw of the various species from log Kow, neutral of the neutral ligand species have slopes between 0.9 and 1. In contrast, the partitioning of the neutral and cationic copper-8-hydroxyquinoline complexes is dependent on several factors including the hydrophobicity of the ligand, the effective molecular size, and the polarization of the complex itself. In consequence, there is no linear relationship between log Klipw of these complexes and log Kow of the neutral species of their ligands. The complexes with very bulky substituents showed a reduced uptake. The Klipw of the nominally neutral complexes, where Cu2+ is coordinated with two ligands, were a factor three to four higher than the Klipw of the positively charged complexes with only one ligand. Although liposome-water partitioning merely describes one element of the uptake process into biological membranes, it is a key process for bioavailability of hydrophobic compounds and, presumably, also plays a crucial role for biological uptake of the described metal organic complexes.

Biological Availability↗
PubMedDate not supplied

Anticalculus and antiplaque activity of 8-hydroxyquinoline sulfate.

The effect of 8-hydroxyquinoline sulfate on the formation of artificial calculi, rat calculus, and dog plaque plus its ability to remove dog plaque were studied. Several chemically related agents were also evaluated for their anticalculus effects. The most effective anticalculus agent was 8-hydroxyquinoline sulfate. At concentrations of 4 or 5%, swabbed over molar teeth, it was essentially equally effective in retarding the formation of rat calculus. Significant (1% level) reduction occurred with concentration as low as 3% in rats. When used so as to mimic mouthrinse use, 4% 8-hydroxyquinoline sulfate also significantly (5% level) reduced formation of calculus in rats. All rats showed normal behavioral and weight-gain patterns. Visual evaluation of oral tissues in the swabbing tests plus visual and histopathological evaluation of oral tissues in the mouthrinse procedure showed 8-hydroxyquinoline sulfate had no irritating or toxic effects. In dogs, the teeth treated with 4% 8-hydroxyquinoline sulfate nine times during a five-day period had 93.7 to 98.4% less buccal plaque than vehicle-treated teeth. The antiplaque effect was considerable in both canines and fourth premolars. In older dogs, teeth treated with 4% 8-hydroxyquinoline sulfate 15 times during a ten-day period had 33 to 46.1% less plaque than when treated with the vehicle. The effect was considerable on canines but slight on fourth premolars. In older dogs after 24 treatments during a 15-day period, 4% 8-hydroxyquinoline sulfate removed 25 to 57.5% of established plaque whereas the vehicle removed 2.5 to 22.5%. Again, 8-hydroxyquinoline sulfate was more effective on canine buccal plaque. These results show that 8-hydroxyquinoline sulfate is an effective anticalculus and antiplaque agent that is nontoxic to animal oral tissue. The results also indicate that the dog is a suitable animal model for the evaluation of antiplaque agents.

Animals↗
PubMed1989

Uptake of 63Ni2+ in the central and peripheral nervous system of mice after oral administration: effects of treatments with halogenated 8-hydroxyquinolines.

Oral administration of 63Ni2+ to mice resulted in higher levels of the metal in the sciatic nerves, the trigeminal ganglia, spinal nerve roots and the spinal cord than in the cerebellum and the frontal cortex. In the sciatic nerves, the trigeminal ganglia and the spinal nerve roots a high vascular permeability may explain the preferential uptake of the 63Ni2+. The higher accumulation of the 63Ni2+ in the spinal cord than in the examined structures of the brain may be related to a diffusion from the cerebrospinal fluid. Administrations of halogenated 8-hydroxyquinolines [5,7-diiodo-8-hydroxyquinoline (diI-HQ), 5,7-dibromo-8-hydroxyquinoline (diBr-HQ), 5,7-dichloro-8-hydroxyquinoline (diCl-HQ) or 5-chloro-7-iodo-8-hydroxyquinoline (Cl-I-HQ)] together with the 63Ni2+ resulted in increased levels of the metal both in neural and extraneural tissues in comparison with mice given the 63Ni2+ alone. In most instances the tissue-levels of 63Ni2+ were 2-4 times higher in the animals treated with the halogenated 8-hydroxyquinolines than in the controls. Determinations of chloroform/water partition coefficients showed that lipophilic chelates are formed between each of these compounds and the nickel. Our results are probably explained by a facilitated passage of the complexed metal over the walls of the stomach and the intestine. The halogenated 8-hydroxyquinolines are linked with the SMON-syndrome, a disease which occurred primarily in Japan. The possibility that this syndrome may be causally connected with a concomitant intake of these drugs and metals is discussed.

Administration, Oral↗
PubMed2002

Antioxidative or prooxidative effect of 4-hydroxyquinoline derivatives on free-radical-initiated hemolysis of erythrocytes is due to its distributive status.

7-Chloro-4-hydroxyquinoline (CQ) is an antitumor drug but its efficiency is not very satisfactory. This fact motivates us to study the relationship between the structure of 4-hydroxyquinoline with various substituent and its antioxidant effect against free-radical-initiated peroxidation: the hemolysis of human erythrocyte initiated thermally by water-soluble initiator, 2,2'-azobis (2-amidinopropane hydrochloride) (AAPH), acts as an experimental system. 7-Fluoro-4-hydroxyquinoline (FQ) and CQ can be synthesized by decarboxylation of 7-fluoro-4-hydroxyquinoline-3-carboxylic acid (FQCA) and 7-chloro-4-hydroxyquinoline-3-carboxylic acid (CQCA), respectively, and FQCA and CQCA are prepared by hydrolysis of ethyl 7-fluoro-4-hydroxyquinoline-3-carboxylate (FQCE) and ethyl 7-chloro-4-hydroxyquinoline-3-carboxylate (CQCE), respectively. The inhibitory concentration of 50% inhibition (IC(50)) of AAPH-induced hemolysis of the erythrocyte has been studied and found that all these chemicals dissolved in dimethyl sulfoxide (DMSO) can inhibit the free-radical-induced peroxidation. To clarify the relationship between the distributive status of the chemicals and their antioxidant effect, the chemical has been dissolved in the vesicle of dipalmitoyl phosphatidylcholine (DPPC) by sonication and suspended in the reaction system. It is found that FQCE, CQCE, FQCA and CQCA act as prooxidants either used alone or used in combination with alpha-tocopherol (TOH), demonstrating that FQCE, CQCE, FQCA and CQCA play a prooxidative role when they are packaged in the DPPC vesicle. This can be understood that the electron-attracting group, i.e. -COOC(2)H(5), -COOH, at the ortho position to the hydroxy group of quinoline makes the phenoxy radical of quinoline derivatives active by attracting negative charge from the electron-deficient radical site. These unstable free radicals preserved in DPPC vesicle can initiate additional propagation of lipid peroxidation and cause hemolysis. However, FQ and CQ without electron-attracting group are antioxidants even in DPPC vesicle either used alone, or mixed with TOH. Moreover, the antioxidative activity of FQ is much better than CQ either used alone or in combination with TOH, indicating that FQ has the potential to replace CQ to be an antioxidant drug. Therefore, the antioxidant/prooxidant effect is not only correlated with the molecular structure but also the distributive status in the reaction system.

1,2-Dipalmitoylphosphatidylcholine↗
PubMed1976

Hydroxyquinolines inhibit ribonucleic acid-dependent deoxyribonucleic acid polymerase and inactivate Rous sarcoma virus and herpes simplex virus.

8-Hydroxyquinoline and several of its derivatives inactivate the transforming ability of Rous sarcoma virus and inhibit its ribonucleic acid-dependent deoxyribonucleic acid polymerase activity. The copper complex of these metal-binding ligands is as active as the free ligand. The activity of the 8-hydroxyquinolines is approximately 50-fold more effective than another group of metal-binding compounds that we have tested, the thiosemicarbazones. In contrast to the potency of the 8-hydroxyquinolines to inactivate Rous sarcoma virus, no intracellular inhibition of transformation could be demonstrated at a concentration that did not affect the growth and appearance of the cells. Cellular deoxyribonucleic acid synthesis was inhibited to a greater extent than was ribonucleic acid or protein synthesis. The phenomenon of "concentration quenching" was observed with high concentrations of drug, causing less inhibition of deoxyribonucleic acid synthesis than was observed with lower concentrations. Herpes simplex virus type 1 was inactivated also by the 8-hydroxyquinolines and their copper complexes. No intracellular inhibition of plaque formation was observed. Treatment with 8-hydroxyquinoline sulfate had no effect on the resolution of herpetic keratitis in rabbits. Some 8-hydroxyquinolines bind to deoxyribonucleic acid in the presence of copper, a phenomenon that may be important in their antiviral activity.

Animals↗
PubMed1977

The significance of the hairpin counter-current principle in the pathogenesis of toxic kidney lesions. An investigation of the influence of antidiuretic hormone and papaverine on hydroxyquinoline nephropathy of the rat.

The influence of antidiuretic hormone (ADH) and papaverine on hydroxyquinoline-induced nephropathy in rats was tested, using histotopochemistry, enzyme activity measurement and morphometric investigation. Hydroxyquinoline causes a marked increase in renal weight, the development of wedge-shaped foci with severely dilated tubule segments, and a simultaneous reduction in dehydrogenases, alkaline phosphatase, and alpha-naphthyl esterase. Both ADH and papaverine produced a significant inhibition of renal damage. The subjective findings were quantitatively confirmed by measurement of enzyme activity, using the microscope photometer, and by morphometric studies with the Leitz-Classimat (determination on the basis of the alkaline phosphatase reaction) of the surface percentage of brush border in the proximal tubules. A disturbance of the hairpin counter-current system is to be considered as the cause of the renal lesion. This disturbance is caused by hydroxyquinoline-induced impairment of Na+/K+ transport, especially in the thick ascending limb of Henle's loop. Our results show that the hydroxyquinoline nephropathy can be favourably influenced both by stimulation of water re-absorption and possibly also transepithelial Na+ transport (ADH), and by increasing the blood flow of the arteriolae rectae with a resultant lowering of the intratubular urine concentration (papaverine). The dependency of hydroxyquinoline nephropathy on the phylogenetically determined concentration capacity of the kidney, and the effective influencing of the condition by ADH and papaverine indicate the importance of the degree of efficiency of the medullary countercurrent system in the pathogenesis of this renal lesion.

Alkaline Phosphatase↗
PubMed1975

The mechanism of inhibition of ribonucleic acid synthesis by 8-hydroxyquinoline and the antibiotic lomofungin.

RNA synthesis in yeast is rapidly inhibited by 8-hydroxyquinoline and the phenazine antibiotic lomofungin (5-formyl-1-methoxycarbonyl-4,6,8-trihydroxyphenazine). It is shown that lomofungin, like 8-hydroxyquinoline, is a chelating agent for bivalent cations. The mechanism of inhibition of RNA synthesis by lomofungin and 8-hydroxyquinoline was investigated in experiments with isolated Escherichia coli RNA polymerase. The results show that both inhibitors are capable of inhibiting polymerase activity solely by chelating the dissociable cations Mn2+ and Mg2+. Evidence is presented which shows that inhibition may occur in the absence of any direct contact between the RNA polymerase or DNA template and the inhibitor. The possibility that inhibition might also occur by chelation of the Zn2+, which is tightly bound to the polymerase, is discussed: it is concluded that lomofungin or 8-hydroxyquinoline is likely to inhibit the enzyme by removal of Mn2+ and Mg2+ before chelating the Zn2+. On the basis of inhibition by chelation of Mn2+ and Mg2+, explanations are proposed for why lomofungin and 8-hydroxyquinoline inhibit synthesis of ribosomal and polydisperse RNA more than that of 5S RNA and tRNA, and for why protein synthesis is not immediately inhibited in the intact yeast cell.

Chelating Agents↗