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PubMed1989

Chloramine-T solutions: effect on wound healing in guinea pigs.

An evaluation of the wound-healing and disinfectant activities of chloramine-T (Chlorazene) used in hydrotherapy whirlpools was studied in a guinea pig cutaneous wound model. Standard microbiologic methods were used to determine the bacteriocidal activity of Chlorazene in cultures containing up to 2.03 x 10(6) colony-forming units per milliliter of Pseudomonas aeruginosa. Full-thickness skin wounds in 40 guinea pigs were inoculated with Pseudomonas aeruginosa and all animals allowed to recover from anesthesia. Twenty-four hours later, animals were placed in water only or water containing Chlorazene (300ppm) for 20 minutes. This procedure was repeated daily for up to seven days after inoculation of wounded skin. Rate of wound epithelialization and number of infected wounds were determined. Large reductions in numbers of cultured organisms were observed after treatment with Chlorazene. No differences in rate of wound healing could be determined in water- or Chlorazene-treated animals. Chlorazene-treated wounds contained fewer pseudomonas organisms than water-treated controls on postinoculation days five and six. These results confirm that Chlorazene is an effective water disinfectant. Data also indicate that in the concentration used, Chlorazene does not affect the rate of wound healing.

Animals↗
PubMed1989

Modification of single sodium channels in neuroblastoma cells by chloramine-T.

We have studied the behaviour of single sodium channels in cell-attached patches in neuroblastoma cell line N1E 115 at 8-15 degrees C modified by chloramine-T (CT). Application of the agent to the external surface of the membrane cause different effects: CT binds to the membrane and cause irreversible effects leading to a decrease of open channel lifetime at 10 or 20 mV relative potentials without affecting the amplitude of single channel current. Channels modified by CT show a tendency to occur in burst (they can open and close several times during depolarization). Therefore, the slower decay of the average current must be explained by the flickering behaviour of the modified channels. We also examined the effect of CT on the relationship between open time of the channels and membrane potential. On the other hand, a small decrease in the mean delay time as a function of membrane voltages was observed which probably is related to the three state model of inactivation. Our results suggest that CT modifies sodium channel inactivation.

Animals↗
PubMed1978

[Hydrogen peroxide, chloramine T and chlorhexidrine in the disinfection of acrylic resin].

The effectiveness of 3% h drogen peroxide, 5% chloramine T and 0,5% chlorhexidine gluconate solutions in disinfection of acrylic resine plates massively infected with oral flora was analysed. The acrylic resine plates used for investigations, were infected in vitro with mixed salivary flora characterized by small numbers of yeast-like fungi (1st group), or great number of these microorganisms (2nd group). Infected plates were exposed to solutions of analysed disinfectants during various time periods. After rinsing or inactivation of disinfectant residues, acrylic plates were put into bacteriological medium and incubated during 7 days period in 37 degrees C. The results of this study indicated the effectiveness of acrylic plates disinfection to be dependent on used disinfectant, time of exposition, and microorganisms present on the surface of acrylic resine. The solutions of disinfectants were less active in the cases of plates infected with material containing great numbers of yeast-like microorganisms. Among analysed disinfectants 0,5% solution of chlorhexidine was characterized by most effective and rapid activity, whereas 3% solution of hydrogen peroxide was found to be the least effective.

Acrylic Resins↗
PubMedDate not supplied

Titrimetric determination of vitamin B6 using chloramine-T, bromamine-T, and bromamine-B.

Simple titrimetric methods have been developed for determination of the vitamin pyridoxine (PRX) in solution, using aromatic N-haloamines, chloramine-T, bromamine-T, and bromamine-B. The method is based on oxidation of PRX by the N-haloamines; the oxidation involves a 2-electron change. The reaction products, pyridoxal and sulfonamides, were identified. The effects of variables, such as pH of the medium and the presence of foreign ions, and pyridoxal, pyridoxalamine, glycerol, and alcohol, on the rate of oxidation were studied. The methods are useful for determining PRX in pharmaceutical formulations and for assaying its cadmium complex. Statistical evaluation showed that analytical results are accurate to within 1%.

Chemical Phenomena↗
PubMed1984

Chlorination of endogenous amines by isolated neutrophils. Ammonia-dependent bactericidal, cytotoxic, and cytolytic activities of the chloramines.

Isolated human neutrophilic leukocytes were stimulated to produce hydrogen peroxide (H2O2) and to secrete cytoplasmic granule components including myeloperoxidase into the medium. Myeloperoxidase catalyzed the oxidation of chloride (Cl-) by H2O2 to yield hypochlorous acid (HOCl), which reacted with endogenous nitrogen compounds to yield derivatives containing nitrogen-chlorine (N-Cl) bonds. Compounds available for reaction with HOCl were ammonia (NH+4), taurine, alpha-amino acids, and granule proteins and peptides that were released into the medium. A portion of the N-Cl derivatives formed under these conditions accumulated in the extracellular medium. These long lived oxidizing agents were characterized as hydrophilic, low molecular weight, mono-N-chloramine (RNHCl) derivatives based on their absorption spectrum, ability to oxidize 5-thio-2-nitrobenzoic acid and to chlorinate ammonia (NH+4), and behavior upon ultrafiltration, gel chromatography, and extraction with organic solvents. The RNHCl derivatives were of low toxicity, but reacted with NH+4 to yield the lipophilic oxidizing agent monochloramine (NH2Cl). Therefore, the addition of NH+4 conferred bactericidal, cytotoxic, and cytolytic activities on the RNHCl derivatives. The results indicate that taurine and other neutrophil amines protect neutrophils and other cells against oxidative attack by acting as a trap for HOCl and by competing with endogenous NH+4 for reaction with HOCl. However, the RNHCl derivatives act as a reserve of oxidizing equivalents that is converted to a toxic form when an increase in NH+4 concentration favors formation of NH2Cl.

Amines↗
PubMedDate not supplied

In vitro and in vivo effects of chloramine T on rat serum elastase inhibitor.

Recent studies have shown that oxidizing agents may block the elastase inhibitory activity of alpha 1-antiproteinase in humans and some animal species. It has been postulated that this protein plays a critical role in modulating the activity of the neutral proteinase, i.e. elastase, in the lung; its inactivation has been implicated in the destruction of lung tissue seen in emphysema. In this work, we have studied the inactivation in vitro of rat serum elastase inhibitor by chloramine T (CT) and whether the in vivo use of the same oxidizing agent in the development of a functional model of alpha 1-antiproteinase deficiency in the rat is feasible. Although serum alpha 1-antiproteinase is readily inactivated in vitro by CT, it was observed, in vivo, that serum elastase inhibitory capacity was reduced to about 28-35% of initial levels 1-3 h after CT injection, and returned to control values within 9 h. Therefore, the in vivo study demonstrated that in the rat a functional model of alpha 1-antiproteinase deficiency cannot be achieved by inactivation of the protein molecule with CT. The relatively short half-life (1.45 h) of the serum elastase inhibitor found in normal rats is consistent with a rapid synthesis of the protein molecule, which might contribute to the fast recovery of the elastase inhibitory capacity observed in experimental animals after CT administration.

Animals↗
PubMed1984

[Substrate reaction concentration in chloramine iodination].

The conditions of chloramine iodization of peptides of different nature have been systematically studied. The empirical formula permitting the calculation of the optimal aliquot of polypeptide without additional experiments is proposed; this method ensures the saturation of peptide molecules with iodine approximately to a level of 1 iodine atom per molecule.

Antigens↗
PubMed1977

Comparison of iodine monochloride and modified chloramine-T radioiodination for in vivo protein studies.

Aggregate formation on gel chromatography and shortened in vivo t1/2 have been shown to result from the usual chloramine-T (CT) radioiodination of proteins. A modified CT method with decreased CT: protein ratio has ben advocated, particularly for use in the 125I-fibrinogen uptake test. In the present study, such modified CT procedures with 131I were assessed by simultaneous injection in rabbits of iodine-125 monochloride protein standards along with the 131I-CT proteins. Standard clearance analyses were performed. For both albumin and fibrinogen a much reduced CT:protein ratio was required before satisfactory in vivo proteins were obtained. The ratio differed for the two proteins, with fibrinogen being more susceptible to CT-induced aggregate formation. Intermediate CT:protein ratios resulted in denaturation of only a portion of the labeled proteins as manifested by a low C1 with a normal t1/2 for the slow component. At intermediate ratios, unaggregated protein displayed abnormal clearance kinetics, indicating that denaturation was not solely the result of aggregates. The results indicated modified CT radioiodination can be used for in vivo studies, but only if carefully compared in vivo with more generally used radiolabeling procedures.

Albumins↗
PubMed1998

[Effect on the microbicidal efficacy of formaldehyde, glutardialdehyde, peracetic acid, chloramine T (N-chloro-4-toluenesulfonamide), m-cresol, ethanol and benzyldimethyldodecacylammonium bromide by blood (model experiments for chemical disinfection of instruments)].

In a preceding paper (Zbl. Hyg. 191 [1991] 457-477) we reported on the dependence of the microbicidal efficacy of active agents of the disinfection of instruments on the amount of coagulated blood adhering to the instruments. In the present investigation, we were interested in the dependence of the microbicidal effects on the amount of blood in the solutions of the active agents. Test areas of 2 cm2 were contaminated with 50 and 100 microliters coagulating blood, respectively, containing cells of Staphylococcus aureus as test germ. The solutions of the microbicidal agents were contaminated with heparinized blood up to a concentration of 4% immediately before starting the disinfection and 24 hours before, respectively. After a period of action lasting 1 hour at 20 degrees C, the relative number of test germs capable of multiplying (N/N0) was determined. The concentration of the microbicidal substances reducing the relative number of test germs capable to multiply to 10(-4) served for estimating the dependence of the microbicidal efficacy of the agents on the blood content of the solutions. The experimental results depended on the thickness of the layer of coagulated blood. The dependence of the efficacy of the microbicidal substances on the blood content of the solutions was the higher the thinner the blood layer was. At a thickness of the layer of the coagulated blood of 0.25 mm, a blood content of the solution of 4%, and applying it immediately after adding the blood, the concentration of glutardialdehyde had to be 1.6 times that without blood to reach the same microbicidal efficacy. When applying the solution 24 hours after adding the blood, the concentration of glutardialdehyde had to be 4.2 times that without blood. The quaternary ammonium compound reacted faster with the blood than did glutardialdehyde; the respective factors were 2.6 and 4.5. The concentration factors of chloramine T were 3.3 and 3.8. Under the conditions of the test, peracetic acid exhibited small concentration factors: 1.3 and 1.6. The microbicidal efficacy of ethanol, formaldehyde and m-cresol soap solution was not or only slightly altered by the amount of blood in the solution of the microbicidal agent.

Benzalkonium Compounds↗
PubMed1999

Taurine chloramine inhibition of cell proliferation and cytokine production by rheumatoid arthritis fibroblast-like synoviocytes.

OBJECTIVE: To examine whether taurine (Tau) or its physiologic chlorinated derivative, taurine chloramine (Tau-CI), affects proliferation of, and proinflammatory cytokine (interleukin-6 [IL-6] and IL-8) production by, fibroblast-like synoviocytes (FLS) isolated from rheumatoid arthritis (RA) patients. METHODS: FLS, isolated from the synovial tissue of 19 RA patients and cultured in vitro for 3-6 passages, were stimulated with the recombinant human cytokines IL-1beta (1 ng/ml), tumor necrosis factor alpha (TNFalpha; 10 ng/ml), or IL-17 (10 ng/ml) in the presence of either Tau or Tau-Cl, which were added at concentrations of 50-500 microM. Tau and Tau-Cl were added simultaneously with, 2 hours before, or 24 hours after the stimuli. The concentrations of IL-6 and IL-8 were determined in culture supernatants using specific enzyme-linked immunosorbent assays. Proliferation of FLS was estimated on the basis of 3H-thymidine incorporation into the cells, which were cultured for 72 hours in the presence of recombinant human basic fibroblast growth factor (bFGF) (1 ng/ml) and Tau or Tau-Cl, which were added simultaneously at the beginning of the culture. RESULTS: Cultured in vitro, RA FLS spontaneously secreted low levels of IL-6 and IL-8, but when RA FLS were stimulated with IL-1beta, TNFalpha, or IL-17, significantly higher amounts of IL-6 and IL-8 were produced. Tau-Cl, but not Tau, inhibited cytokine-triggered synthesis of IL-6 (50% inhibitory concentration [IC50] approximately 225 microM) and IL-8 (IC50 approximately 450 microM) when added simultaneously with the stimuli. However, IL-17-induced production of IL-8 was not affected by Tau-Cl. In the cells prestimulated with IL-1beta for 24 hours, Tau-Cl still inhibited synthesis of IL-6, but did not affect IL-8 production. Moreover, Tau-Cl inhibited spontaneous and bFGF-triggered proliferation of FLS in a dose-dependent manner. Neither Tau nor Tau-Cl affected cell viability. CONCLUSION: The results of these studies demonstrate that Tau-Cl inhibits production of proinflammatory cytokines by RA FLS, as well as proliferation of these cells. Thus, Tau-Cl may act as a physiologic modulator of FLS functions related to their pathogenic role in RA.

Adult↗
PubMed2000

The mechanism of taurine chloramine inhibition of cytokine (interleukin-6, interleukin-8) production by rheumatoid arthritis fibroblast-like synoviocytes.

OBJECTIVE: Taurine chloramine (Tau-Cl) has been shown to inhibit the production of proinflammatory cytokines (interleukin-6 [IL-6] and IL-8) by fibroblast-like synoviocytes (FLS) isolated from rheumatoid arthritis (RA) patients. The present study was conducted to elucidate the mechanism of inhibitory action exerted by Tau-Cl. METHODS: The effects of Tau-Cl on 1) the transcription of genes coding for IL-6 and IL-8, and 2) the activity of nuclear factor kappaB (NF-kappaB) and activator protein 1 (AP-1) transcription factors, which are crucial for the transcription of these cytokine genes, were investigated in FLS isolated from the synovial tissue of RA patients. FLS were cultured in vitro for 3-6 passages and stimulated with recombinant human IL-1beta (1 ng/ml) in the presence of either Tau or Tau-Cl, which were added simultaneously with the stimulus at concentrations of 250 microM or 500 microM. The relative expression of IL-6 and IL-8 messenger RNA (mRNA) was evaluated after 4 hours of stimulation, using competitive reverse transcriptase-polymerase chain reaction. The DNA binding activity of NF-kappaB and AP-1 was examined 30 minutes and 2 hours after cell stimulation, respectively, using electromobility gel shift assay. RESULTS: IL-1beta triggered a significant rise in the activity of transcription factors NF-kappaB and AP-1, followed by an elevation of cytokine IL-6 and IL-8 mRNA expression. Tau-Cl, but not Tau, reduced IL-1beta-triggered cytokine mRNA expression, exerting stronger inhibitory activity on the levels of IL-6 than on those of IL-8. Importantly, Tau-Cl also diminished the activity of NF-kappaB and, to a lesser extent, that of AP-1 transcription factor. Neither IL-1beta nor Tau-Cl affected the activity of octamer transcription factor 1. CONCLUSION: Tau-Cl inhibition of IL-6 and IL-8 synthesis in FLS from RA patients results from the ability of this compound to diminish the activity of the major transcriptional regulators (NF-kappaB and AP-1), which subsequently reduces the transcription of these cytokine genes.

Aged↗
PubMed2003

Selective inhibition of cyclooxygenase 2-generated prostaglandin E2 synthesis in rheumatoid arthritis synoviocytes by taurine chloramine.

OBJECTIVE: To investigate the effects of taurine chloramine (Tau-Cl), a chlorinated derivative of the amino acid taurine, on the expression of cyclooxygenase (COX) isoenzymes and prostaglandin E(2) (PGE(2)) synthesis in rheumatoid arthritis (RA) fibroblast-like synoviocytes (FLS). METHODS: FLS, isolated from the synovial tissue of RA patients, were treated in vitro with either interleukin-1beta (IL-1beta; 1 ng/ml) alone or together with 200-500 microM Tau-Cl. The expression of COX isoenzymes was evaluated at both the protein (Western blotting) and the messenger RNA (mRNA) (reverse transcriptase-polymerase chain reaction) levels. The concentration of PGE(2) was measured by competitive acetylcholinesterase enzyme immunoassay. RESULTS: Resting FLS expressed mRNA encoding both COX-1 and COX-2, but only COX-1 was present at the protein level. These cells produced negligible amounts of PGE(2). Upon stimulation with IL-1beta, elevation of COX-2, but not COX-1, mRNA and protein preceded the enhancement of PGE(2) synthesis. In the presence of 300-400 microM Tau-Cl, significant inhibition of IL-1beta-triggered COX-2 mRNA and protein, and a related decrease in PGE(2) production, was observed. In contrast, no significant changes in COX-1 mRNA and protein levels were noted. CONCLUSION: Tau-Cl inhibits IL-1beta-triggered elevation of COX-2 and generation of PGE(2) by RA FLS. These results expand the spectrum of known antiinflammatory activities of this compound.

Arthritis, Rheumatoid↗
PubMed1993

Taurine chloramine inhibits the synthesis of nitric oxide and the release of tumor necrosis factor in activated RAW 264.7 cells.

Taurine is present in high concentrations in most mammalian tissues, including those that prodigiously produce oxidants. Taurine protects against bronchiolar damage induced by NO2, ozone, bleomycin, and amiodarone. Taurine is chlorinated to form taurine chloramine (Tau-Cl) by the halide-dependent myeloperoxidase system and, under physiological conditions, reduces HOCl toxicity. Although NO and its metabolites, NO2- and NO3-, are thought to be major mediators of tissue damage resulting from oxidant exposure, cytokines, including tumor necrosis factor (TNF), are also involved. We examined the effects of Tau-Cl on NO production and TNF release by using RAW 264.7 cells activated with recombinant interferon-gamma (rIFN-gamma; 50 U/ml) and lipopolysaccharide (LPS; 10 micrograms/ml). NO was measured spectrophotometrically as NO2- after reaction with Griess reagent and TNF was measured by ELISA. Tau-Cl (0.5 mM) inhibits NO and TNF released into the medium by 47% and 43%, respectively. Tau-Cl is actively transported into RAW 264.7 cells by an uptake system that is energy, temperature, and Na+ dependent. Competition experiments demonstrate that the uptake system for Tau-Cl is distinct from that for taurine. In addition, the NO synthase activity of cytosolic preparations from activated RAW 264.7 cells is irreversibly inhibited by pretreatment with Tau-Cl. We demonstrate that Tau-Cl inhibits production of NO and TNF by activated macrophages and suggest a mechanism through which taurine supplementation may protect against oxidant-induced tissue damage.

Amino Acid Oxidoreductases↗
PubMed2002

Taurine chloramine inhibits lymphocyte proliferation and decreases cytokine production in activated human leukocytes.

Previously, we described the inhibition of proinflammatory mediators such as nitric oxide, tumor necrosis factor-alpha (TNF-alpha), and prostaglandin E2 by taurine chloramine (Tau-Cl) in activated rodent macrophages. We also demonstrated that Tau-Cl suppressed superoxide anion, IL-6, and IL-8 production in activated human polymorphonuclear leukocytes separated from peripheral blood. In these studies, we report the effect of Tau-Cl on lymphocyte proliferation and the production of cytokines by activated human peripheral blood mononuclear leukocytes. Adherent and nonadherent leukocytes were activated using lipopolysaccharide (LPS) and phytohemagglutinin (PHA), respectively, in the presence or absence of Tau-Cl. Tau-Cl significantly suppressed lymphocyte proliferation as measured by tritiated (3H) thymidine. Production of IL-6, IL-8, and IL-2 in PHA-activated nonadherent leukocytes was inhibited by Tau-Cl. The production of IL-1beta, IL-6, and IL-8 was also decreased in LPS-activated adherent monocytes by Tau-Cl. These data demonstrate that the ability of Tau-Cl to modulate the immune response is not species specific and extends to human leukocytes.

Humans↗
PubMed2006

Taurine chloramine inhibits proliferation of rheumatoid arthritis synoviocytes by triggering a p53-dependent pathway.

OBJECTIVE AND DESIGN: Taurine chloramine (Tau-Cl), originating from activated neutrophils, possesses antiinflammatory activities. Fibroblast-like synoviocytes (FLS) participate in the chronic synovitis and synovial membrane hyperplasia that are characteristic pathological features of rheumatoid arthritis (RA). The present study was conducted to investigate the mechanism of the Tau-Cl effect on the proliferation of these cells in culture. MATERIALS AND METHODS: FLS were stimulated in vitro with platelet derived growth factor (PDGF) alone or together with Tau-Cl. Cell proliferation was evaluated by counting the total and dividing cell numbers and by measurement of (3)H-thymidine incorporation. Expression of the key cell-cycle regulators was evaluated at the protein (Western blotting) and/or mRNA (RT-PCR) levels. RESULTS: Treatment of RA FLS with Tau-Cl (200-500 microM) resulted in an early nuclear accumulation of p53 tumor suppressor protein. Moreover, Tau-Cl inhibited PDGF-triggered cell proliferation (IC(50) value approximately 250-300 microM), accompanied by characteristic modulation of p53 transcriptional targets: down-regulation of proliferating cell nuclear antigen (PCNA) and survivin, and concomitant up-regulation of p21 mitotic inhibitor. CONCLUSION: We propose that Tau-Cl inhibits proliferation of RA FLS by triggering a p53-dependent cell-cycle arrest and conclude that this compound suppresses pathways in FLS that are known to contribute to the pathology of RA.

Anti-Inflammatory Agents↗
PubMed2002

Taurine chloramine modulates cytokine production by human peripheral blood mononuclear cells.

The effect of taurine (Tau) and taurine chloramine (Tau-Cl) on the production of TNF- alpha, IL-1 beta, and IL-6 by peripheral blood mononuclear cells of healthy volunteers was examined. Cells were stimulated with bacterial lipopolysaccharide (LPS) in the presence of either Tau or Tau-Cl. After 24 h culture the cytokine concentrations were measured in both culture supernatants (secreted) and cell lysates (cell-associated) using ELISA. In LPS-stimulated cells Tau-Cl inhibited both the secreted and cell-associated IL-1 beta and IL-6, while exerted dual effect on TNF- alpha production: raising it slightly at low and reducing at higher concentration. By contrast, Tau had no significant effect on the cytokine production. These results indicate that Tau-Cl modulates synthesis of pro-inflammatory cytokines, and therefore it may play a role in the initiation and propagation of immune response.

Adult↗
PubMed2002

Impaired generation of taurine chloramine by synovial fluid neutrophils of rheumatoid arthritis patients.

Taurine (Tau), a dominant free amino acid present in neutrophil cytoplasm, serves as a scavenger for hypochlorous acid (HOCl) released during these cells activation. The resulting taurine chloramine (Tau-Cl) exerts potent anti-inflammatory properties. In the present study we tested the hypothesis that the formation of Tau-Cl is impaired in neutrophils isolated from rheumatoid arthritis (RA) patients. The inhibition of zymosan-triggered chemiluminescence in the presence of exogenous Tau was used for indirect measurement of Tau-Cl generation. The chemiluminescence of neutrophils isolated from peripheral blood (PB) of healthy volunteers and RA patients was inhibited by Tau with similar potency. By contrast, synovial fluid (SF) neutrophils of these patients were significantly less sensitive for Tau-mediated inhibition. Therefore, our data indicate impaired generation of Tau-Cl in neutrophils isolated from SF of RA patients.

Adult↗
PubMed2002

Effect of taurine chloramine, the product of activated neutrophils, on the development of collagen-induced arthritis in DBA 1/J mice.

Taurine chloramine (TauCl), a product of neutrophil myeloperoxidase - halide system, formed by a reaction of taurine with HOCl, is known as an anti-microbial and anti-inflammatory long-lived oxidant. We previously reported that TauCl inhibits in vitro the production of proinflammatory cytokines (IL-6, IL-8) by RA synoviocytes. Therefore we performed this study to investigate the effect of TauCl treatment on the development of collagen-induced arthritis (CIA) in DBA1/J mice. Early administration of TauCl (after primary immunization) resulted in the delay of the onset of CIA, but had no effect on severity of arthritis. TauCl, given daily for 21 days after booster immunization, did not reduce the symptoms of arthritis in those mice, which already developed CIA, but significantly diminished incidence of the disease (55% vs. 90% of placebo mice). The mechanism of this effect is unknown. This is the first in vivo study suggesting that TauCl may be used for immune intervention in chronic inflammatory diseases.

Animals↗