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PubMed1978

Predisposing and operative factors: effect on the incidence of localized osteitis in mandibular third-molar surgery.

Five hundred and four bilateral mandibular third-molar extraction sites were examined postoperatively for localized osteitis. All sites received a mechanical lavage of either 350 ml, or 175 ml. of sterile normal saline solution. No significant differences were observed relative to the effect of lavage volume on the incidence of iocalized osteitis. A preoperative antimicrobial mouthrinse of chloramine-T (sodium-p-toluene sulfonchloramide) was also used by one half of the patients. Although only slight differences were noted in healing with the different lavage volumes of the chloramine-T, certain predisposing factors contributed significant differences.

Adolescent↗
PubMed1989

Oxidized fibrin(ogen) derivatives enhance the activity of tissue type plasminogen activator.

Oxidation of fibrinogen degradation products (FDP) with chloramines, results in a five- fold increase of their property to stimulate plasminogen activation by tissue type plasminogen activator (t-PA). Binding studies with immobilized stimulators demonstrated greater affinity of t-PA to oxidized than to unmodified FDP. The fibrin (ogen) domain responsible for this oxidant mediated increase in t-PA stimulation is localized in the D- subunit of fibrin(ogen). Thus, experimental data with (oxidized) I-labelled fibrin(ogen) should be interpreted with caution: the oxidized product might behave in a distinct manner than the unoxidized, native, one. As activated leukocytes release large amounts of oxidants of the chloramine type (Weiss et al., Science 222, 625-628, 1983), oxidation of fibrin might contribute significantly to fibrinolysis and proteolysis in areas of inflammation. The data give further evidence for an involvement of physiological components of haemostasis in non haemostasis but inflammation related processes.

Chloramines↗
PubMed1991

Nonradical excited oxygen species induce selective thrombolysis in vivo.

All the thrombolytic agents currently in clinical use act as plasminogen activators. In this study evidence is presented that also oxidants of the phagocyte type are of fibrinolytic efficiency in vivo. Activated phagocytes participate in physiologic fibrinolysis. The cells generate plasminogen activators and reactive oxidants of the nitrogen-chlorine type. Experimental mimicry of this oxidative inflammatory response induces selective thrombolysis in a rabbit jugular vein model. Intravenous bolus administration of sub-millimolar blood concentrations of chloramine-T resulted in thrombolysis after about 30 min without notable systemic toxicity; the coagulation parameters activated partial thromboplastin time (aPTT), thrombin time, fibrinogen, and alpha-2-antiplasmin were not influenced. Control experiments with 2000 IU of urokinase/kg induced thrombolysis after about 90 min with systemic changes of the hemostatic system. The fibrinolysis promoting effect of the oxidants of the phagocyte type could be inhibited by quenchers of singlet molecular oxygen and was not affected at all by inhibitors of oxygen radicals. The data gives evidence that nonradical excited oxygen species (NEOS) act as powerful pro-fibrinolytic and anti-coagulant agents in vivo. It might be suggested that NEOS could represent a novel class of regulators of the fibrinolytic system. The long lived and hydrophilic chloramine derivatives can either accumulate or diffuse far from their site of generation. Therefore, on the one hand oxidants in high (local) concentrations might be considered as direct pro-fibrinolytic agents due to their powerful protein modulating efficacy. On the other hand, oxidants at low concentrations may act as indirect pro-fibrinolytic compounds, i.e. as chemoattractants to concentrate phagocytes to the site of a thrombus. In this case the oxidants would play the role of signal elements faraway from the thrombus, a self amplifying mechanism possibly mediated by oxidation of blood arachidonat/lipid metabolites.

Animals↗
PubMed1985

An evaluation of different methods for labelling the surface of the filarial nematode Brugia pahangi with 125iodine.

The specificity of a range of 125I labelling techniques (Chloramine T, Iodogen, Bolton and Hunter reagent, lactoperoxidase and iodosulfanilic acid) to the surface of the filarial nematode Brugia pahangi was evaluated by autoradiography of sections of labelled worms and of dried SDS-polyacrylamide gels following electrophoresis of homogenised worm extracts. It was concluded that Bolton and Hunter reagent was not surface specific but labelled proteins throughout the body of the worm. At the light microscope level autoradiography of worms labelled using Chloramine T, Iodogen, lactoperoxidase and iodosulfanilic acid demonstrated that the 125I labelling was restricted to the worm surface. Electrophoresis and autoradiography showed that each method produced a different pattern of labelled polypeptide. A polypeptide of molecular weight 30 kDa was labelled using each method except Bolton and Hunter reagent, and appears to be a major surface component.

Animals↗
PubMed1991

Inactivation of enzymes and an enzyme inhibitor by oxidative modification with chlorinated amines and metal-catalyzed oxidation systems.

Oxidative inactivation of various key enzymes and alpha-1-proteinase inhibitor (alpha-1-PI) was studied by treatment with N-chloramines and the metal-catalyzed oxidation (MCO)-systems ascorbate/Fe(III) and ascorbate/Cu(II). Chlorinated amines completely inhibited alpha-1-PI, fructose-1,6-bis phosphatase (Fru-P2ase) and glyceraldehyde phosphate dehydrogenase (GAPD) at a low molar excess, and glucose-6-phosphate dehydrogenase (G6PD) at a high molar excess, but did not impair beta-N-acetylglucosaminidase (beta-NAG), alkaline phosphatase (AP) or lactate dehydrogenase (LDH). MCO-systems affected the activities of Fru-P2ase, GAPD, AP, LDH and G6PD, but not those of beta-NAG or alpha-1-PI. EDTA prevented inactivation of Fru-P2ase, G6PD and LDH by ascorbate/Cu(II) and of Fru-P2ase by ascorbate/Fe(III) suggesting a site-specific oxidation catalyzed by a protein-bound metal ion. In conclusion, N-chloramines and MCO-systems exhibited different properties with regard to oxidative inactivation, sulfhydryl-enzymes were susceptible to both systems, but other enzymes were only susceptible to one or neither system.

Alkaline Phosphatase↗
PubMed1986

Antiseptic toxicity in wounds healing by secondary intention.

The effects of two commonly used antiseptics for chronic ulcer care, chloramine T and chlorhexidine, on the biochemical and histological parameters of healing have been examined. The antiseptics were compared with saline when applied to 10 mm skin defects on Sprague-Dawley rats. Chloramine T significantly delayed the production of collagen and prolonged the acute inflammatory response compared with saline. Chlorhexidine did not differ from saline. We conclude that hypochlorite antiseptics may adversely affect healing by secondary intention and the antibacterial and desloughing action of agents should be carefully balanced against their toxic effect.

Animals↗
PubMed1989

Oxidative damage in the guinea pig hippocampal slice.

Free radicals and active oxygen compounds are implicated in brain ischemia and head trauma. Previous studies have shown that free radicals, generated by radiation and through the Fenton reaction, produce both synaptic and postsynaptic damage in the hippocampal brain slice. To evaluate the contribution of oxidation to the observed damage, the actions of the oxidants, chloramine-T and N-chlorosuccinimide (NCS), were studied on electrophysiological responses in the hippocampal slice isolated from the brains of guinea pigs. Electrical stimulation of afferents to neurons of the CA1 region of hippocampus evoked a population postsynaptic potential (population PSP) in the dendritic layer and a population spike in the cell body layer. Chloramine-T (25-500 microM) and NCS (750-4000 microM) decreased the population spike in a dose-dependent manner (ED50 congruent to 125 microM and 1100 microM, respectively). Input/output curves revealed that both the population PSP were significantly reduced with both oxidants; but, the ability of the population PSP to produce a population spike was not impaired. These studies suggest that oxidation reactions can account for the synaptic component of the damage produced by free radicals but can not account for the postsynaptic effects.

Animals↗
PubMed1993

Effect of oxidative stress on excitatory amino acid release by cerebral cortical synaptosomes.

Previous studies in our laboratory have suggested that an oxidation reaction is responsible for the actions of free radicals to decrease synaptic potentials. Recently we observed that free radicals both decreased depolarization-induced vesicular release and enhanced basal, nonvesicular release of the excitatory amino acid, [3H]L-glutamate. In order to evaluate the contribution of oxidative reactions to this latter effect, we evaluated the actions of the oxidizing agent chloramine-T on synaptosomal release of excitatory amino acids, using [3H]D-aspartate as the exogenous label. Basal and depolarization evoked [3H]D-aspartate release were calcium-independent and nonvesicular. Chloramine-T pretreatment significantly increased basal release, while having no effect on high K(+)-evoked release. These data suggest that an oxidative process can mimic the free radical increase of basal release, as well as the decrease in synaptic potentials. On the other hand, the calcium-independent-evoked release may involve a different mechanism. Our results demonstrate that under basal, nondepolarizing conditions, oxidative stress exerts an adverse effect on the presynaptic nerve terminal, resulting in an increased release of potentially damaging excitatory amino acid neurotransmitters.

Amino Acids↗
PubMed2006

Monochloramine potently inhibits arachidonic acid metabolism in rat platelets.

In the present study, the effects of hypochlorous acid (HOCl), monochloramine (NH(2)Cl), glutamine-chloramine (Glu-Cl) and taurine-chloramine (Tau-Cl) on the formation of 12-lipoxygenase (LOX) metabolite, 12-HETE, and cyclooxygenase (COX) metabolites, TXB(2), and 12-HHT, from exogenous arachidonic acid (AA) in rat platelets were examined. Rat platelets (4x10(8)/ml) were preincubated with drugs for 5min at 37 degrees C prior to the incubation with AA (40microM) for 2min at 37 degrees C. HOCl (50-250microM) showed an inhibition on the formation of LOX metabolite (12-HETE, 5-67% inhibition) and COX metabolites (TXB(2), 33-73% inhibition; 12-HHT, 27-74% inhibition). Although Tau-Cl and Glu-Cl up to 100microM were without effect on the formation of 12-HETE, TXB(2) and 12-HTT, NH(2)Cl showed a strong inhibition on the formation of all three metabolites (10-100microM NH(2)Cl, 12-HETE, 21-92% inhibition; TXB(2), 58-94% inhibition; 12-HHT, 36-92% inhibition). Methionine reversed a reduction of formation of LOX and COX metabolites induced by NH(2)Cl, and taurine restoring that induced by both NH(2)Cl and HOCl. These results suggest that NH(2)Cl is a more potent inhibitor of COX and LOX pathways in platelets than HOCl, and taurine and methionine can be modulators of NH(2)Cl-induced alterations in the COX and LOX pathways in vivo.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed2004

Validating sample preservation techniques and holding times for the approved compliance monitoring methods for haloacetic acids under the US EPA's stage 1 D/DBP rule.

Haloacetic acids (HAAs), which are formed during the disinfection of drinking waters with chlorine, are regulated by the US Environmental Protection Agency (EPA) under the Stage 1 Disinfectant/Disinfection Byproducts (D/DBP) Rule. Recently, three studies have been reported indicating that low concentrations of HAAs can also be formed during disinfection with chloramines. Methods currently approved for compliance monitoring under the Stage 1 Rule arrest the chlorine-mediated formation of HAAs by adding ammonium chloride, which forms chloramines. Studies were undertaken using an in-process water that favored the formation of HAAs with moderate total organic carbon concentration and high levels of chlorine to investigate the potential formation of HAAs under sample storage conditions. The ammonium chloride-quenched sample did form a small amount of HAAs, but total formation over a period equal to the 14-day sample storage time was less than 2 microg/l, whereas the unquenched samples increased 41 microg/l during the same period. Pour plate studies indicated that chlorinated drinking waters quenched with ammonium chloride are protected from microbial growth, which is an important additional advantage to this preservation scheme. The presence of a combined chlorine residual should prevent microbial degradation of HAAs in samples. These studies support the preservation protocols and the sample storage times promulgated for compliance monitoring under the Stage 1 D/DBP Rule.

Acetic Acid↗
PubMed2006

Modeling dichloroacetic acid formation from the reaction of monochloramine with natural organic matter.

A kinetic model was developed to predict dichloroacetic acid (DCAA) formation in chloraminated systems. Equations describing DCAA formation were incorporated into an established comprehensive monochloramine-natural organic matter (NOM) reaction model. DCAA formation was theorized to be proportional to the amount of NOM oxidized by monochloramine and described by a single dimensionless DCAA formation coefficient, theta(DCAA) (M(DCAA)/M(DOC(ox)). The applicability of the model to describe DCAA formation in the presence of six different NOM sources was evaluated. DCAA formation could be described by considering a single NOM source-specific value for theta(DCAA) over a wide range of experimental conditions (i.e., pH, NOM, free ammonia, and monochloramine concentrations). DCAA formation appears to be directly proportional to the amount of active chlorine (monochloramine and free chlorine) that reacted with the NOM under these experimental conditions. Values of theta(DCAA) for all six NOM sources, determined by nonlinear regression analysis, varied from 6.51 x 10(-3) to 1.15 x 10(-2) and were linearly correlated with specific ultraviolet absorbance at 280 nm (SUVA(280)). The ability to model monochloramine loss and DCAA formation in the presence of NOM provides insight into disinfection by-product (DBP) formation pathways under chloramination conditions. The subsequent model and correlations to SUVA has the potential to aid the water treatment industry as a tool in developing strategies that minimize DBP formation while maintaining the microbial integrity of the water distribution system.

Chloramines↗
PubMed1998

Differential reactivities of hypochlorous and hypobromous acids with purified Escherichia coli phospholipid: formation of haloamines and halohydrins.

Hypochlorous (HOCl) and hypobromous (HOBr) acids are strong oxidants derived from myeloperoxidase and eosinophil peroxidase, the major antimicrobial enzymes of neutrophils and eosinophils, respectively. These oxidants are highly reactive with a wide range of biomolecules. At physiological pH, both HOCl and HOBr react readily with amines to form haloamines and with the unsaturated bonds of fatty acids to form halohydrins. We have investigated which of these reactions occur with phosphatidylethanolamine (PE), the predominant phospholipid of Escherichia coli. The formation of haloamines was determined by TLC and colorimetrically and the formation of halohydrins was determined by TLC and GC-MS. With HOCl, chloramines were much the preferred product and chlorohydrins were formed in substantial amounts only when HOCl was in excess of the amount required to convert the amine to the dichloramine. With HOBr at all concentrations, bromamines and bromohydrins were formed concurrently, indicating a greater relative reactivity with unsaturated fatty acids than with HOCl. The bromamine derivatives of PE, and other primary amines, were found to be more reactive than the equivalent chloramines, and were able to brominate the unsaturated bonds of fatty acids. Bromohydrins (formed directly or through the action of bromamines) may, therefore, be suitable biomarkers for the production of HOBr in vivo.

Alcohols↗
PubMed1988

Batrachotoxin uncouples gating charge immobilization from fast Na inactivation in squid giant axons.

The fast inactivation of sodium currents and the immobolization of sodium gating charge are thought to be closely coupled to each other. This notion was tested in the squid axon in which kinetics and steady-state properties of the gating charge movement were compared before and after removal of the Na inactivation by batrachotoxin (BTX), pronase, or chloramine-T. The immobilization of gating charge was determined by measuring the total charge movement (QON) obtained by integrating the ON gating current (Ig,ON) using a double pulse protocol. After removal of the fast inactivation with pronase or chloramine-T, the gating charge movement was no longer immobilized. In contrast, after BTX modification, the channels still exhibited an immobilization of the gating charge (QON) with an onset time course and voltage dependence similar to that for the activation process. These results show that BTX can uncouple the charge immobilization from the fast Na inactivation mechanism, suggesting that the Na gating charge movement can be immobilized independently of the inactivation of the channel.

Animals↗
PubMed1998

Kinetics and mechanism of oxidation of erythro-series pentoses and hexoses by N-chloro-p-toluenesulfonamide.

The kinetics and mechanism of oxidation of D-glucose, D-mannose, D-fructose, D-arabinose, and D-ribose with chloramine-T in alkaline medium were studied. The rate law, rate = k [Chloramine-T] [Sugar] [HO-]2, was observed. The rate of the reaction was influenced by a change in ionic strength of the medium, and the dielectric effect was found to be negative. The latter enabled the computation of dAB, the size of the activated complex. The reaction rate was almost doubled in deuterium oxide. Activation energies were calculated from the Arrhenius plots. HPLC and GLC-MS analyses of the products indicated that the sugars were oxidized to a mixture of aldonic acids, consisting of arabinonic, ribonic, erythronic, and glyceric acids. Based on these data, a plausible mechanism involving the aldo-enolic anions of pentoses and keto-enolic anions of hexoses is suggested.

Chemical Phenomena↗
PubMed1997

The effect of chemical anti-inhibitors on fibrinolytic enzymes and inhibitors.

Fibrinolytic enzyme inhibitors hamper the determination of the specific fibrinolytic serine protease activity. Reportedly, chemical anti-inhibitors eliminate the influence of fibrinolytic inhibitors, but it remains unclear to what extent they change the specific activity of fibrinolytic serine proteases. We studied the influence of chemical anti-inhibitors (chloramine T, flufenamate, sodium lauryl sulfate, and methylamine) on fibrinolytic serine proteases and fibrinolytic enzyme inhibitors using the physiological substrate fibrin as plasmin substrate. Low concentrations of chloramine T (0.01 mmol/l) prevent the inhibition of plasminogen activators. Higher concentrations (1 mmol/l) reduce the inhibition of plasmin, but simultaneously quench the plasminogen activator activity. Flufenamate eliminates most fibrinolytic enzyme inhibitors, but increases the activity of plasmin (apparent recovery 140%) and plasminogen activators (apparent recovery > 200%). Sodium lauryl sulfate eliminates the major fibrinolytic enzyme inhibitors, but increases the activity of plasmin (apparent recovery > 200%) and plasminogen activator, urokinase type (apparent recovery 130%). Methylamine affects only plasmin inhibition. We conclude that chemical anti-inhibitors may invalidate the analytical specificity of methods for the determination of fibrinolytic serine protease activity.

Chloramines↗
PubMed2002

Superoxide radicals can act synergistically with hypochlorite to induce damage to proteins.

Activated phagocytes generate both superoxide radicals via a respiratory burst, and HOCl via the concurrent release of the haem enzyme myeloperoxidase. Amine and amide functions on proteins and carbohydrates are major targets for HOCl, generating chloramines (RNHCl) and chloramides (RC(O)NClR'), which can accumulate to high concentrations (>100 microM). Here we show that superoxide radicals catalyse the decomposition of chloramines and chloramides to reactive nitrogen-centred radicals, and increase the extent of protein fragmentation compared to that observed with either superoxide radicals or HOCl, alone. This synergistic action may be of significance at sites of inflammation, where both superoxide radicals and chloramines/chloramides are formed simultaneously.

Chloramines↗
PubMed2001

Determination of nutrients limiting biofilm formation and the subsequent impact on disinfectant decay.

Understanding the contribution of both organic and inorganic nutrients to biofilm development and the subsequent impact of developed biofilms on disinfectant decay are important requirements for distribution system management strategies. Nutrient limitation may be one way to control biofilm development without increasing disinfectant dosing. Little is known, however, of the nutrient requirements of biofilms in distribution systems. Indeed, the effects on biofilm development due to the addition of nutrients to distribution systems and what impact biofilm development may have on disinfectant decay is still poorly understood. This study used annular reactors to determine the nutrients limiting for biofilm development in drinking water from two different Sydney sources and the subsequent effects of biofilm development on disinfectant decay. It was found that biofilm development in Sydney water was limited by organic carbon and that biofilm development promoted chloramine decay. Moreover, biofilm development occurred in the presence of chloramine. The ability of biofilms to respond to increases in disinfectant concentrations was dependent on the biomass of the biofilms. In a comparative study using chlorinated drinking water containing very low levels of organic carbon, biofilm development was not detected. Removal of organic carbon resulted in greater persistence of chlorine, which led to greater biofilm control. It was also shown that biofilms could contribute cells to the aqueous phase. The results of the study indicate that treatment and system management strategies should incorporate organic carbon removal to limit biofilm development through a combination of retarding bacterial growth and enhancing disinfectant persistence.

Australia↗
PubMed1992

Activation of the fifth component of human complement by oxygen-derived free radicals, and by methionine oxidizing agents: a comparison.

The fifth component of human complement, C5, was activated by non-enzymical, chemical treatment in either of two ways: 1) by oxidation with a hydroxyl radical (OH.) generating system consisting of H2O2, FeEDTA, and ascorbate, activation product called C5(H2O2); 2) by oxidation with chloramine T, activation product called C5(Cl-T). Evaluating earlier findings, completed by new results, both products were compared. Both products are C5-like in that they are capable of binding C6 and form the nucleus for the cytotoxic complex C5-9. Both differ from C5b, the natural activation product of C5, as they comprise the whole, uncleaved C5 protein, and do not immediately decay when not bound to C6. In both cases the treatment involves oxidation of methionine residues in the C5 protein. However, while chloramine T specifically attacks only methionine, oxidation by the OH. generating system involves other amino acid residues, in addition. This probably explains the lower yield of C5b-like activity after treatment with H2O2, and other quantitative differences between C5(H2O2) and C5(Cl-T). Whereas the generation of C5(H2O2) may be physiologically relevant, C5(Cl-T) may prove to be a suitable object for the study of changes in the C5 molecule essential for its activation.

Chloramines↗