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PubMed1995

[125I]IgM (KAU) human monoclonal cold agglutinin: labelling and studies on its biological activity.

In order to study the interaction between an IgM cold agglutinin and the erythrocyte I antigen, the former antibody was labelled with 125I using the Chloramine-T, IODOGEN and Bolton-Hunter methods. High incorporation and adequate stability of the labelled IgM were obtained with all procedures. However, suitable biological activity was maintained only with the Bolton-Hunter method. Further studies suggest that tyrosine iodination affects antigen recognition by this IgM, whereas iodination of amino groups does not. The reagent thus prepared allowed the determination of the number of I sites per erythrocyte as well as the antibody affinity constant.

Adult↗
PubMed2005

Oxidative modification of IkappaB by monochloramine inhibits tumor necrosis factor alpha-induced NF-kappaB activation.

We have previously reported that monochloramine (NH(2)Cl), a neutrophil-derived oxidant, inhibited tumor necrosis factor alpha (TNFalpha)-induced expression of cell adhesion molecules and nuclear factor-kappaB (NF-kappaB) activation (Free Radical Research 36 (2002) 845-852). Here, we studied the mechanism how NH(2)Cl inhibited TNFalpha-induced NF-kappaB activation, and compared the effects with taurine chloramine (Tau-NHCl). Pretreatment of Jurkat cells with NH(2)Cl at 70 microM resulted in suppression of TNFalpha-induced IkappaB phosphorylation and degradation, and inhibited NF-kappaB activation. In addition, a slow-moving IkappaB band appeared on SDS-PAGE. By contrast, Tau-NHCl for up to 200 microM had no effects. Interestingly, NH(2)Cl did not inhibit IkappaB kinase activation by TNFalpha. Protein phosphatase activity did not show apparent change. When recombinant IkappaB was oxidized by NH(2)Cl in vitro and phosphorylated by TNFalpha-stimulated Jurkat cell lysate, its phosphorylation occurred less effectively than non-oxidized IkappaB. In addition, when NF-kappaB-IkappaB complex was immunoprecipitated from NH(2)Cl-treated cells and phosphorylated in vitro by recombinant active IkappaB kinase, native IkappaB but not oxidized IkappaB was phosphorylated. Amino acid analysis of the in vitro oxidized IkappaB showed methionine oxidation to methionine sulfoxide. Although Tau-NHCl alone had little effects on TNFalpha-induced NF-kappaB activation, simultaneous presence of Tau-NHCl and ammonium ion significantly inhibited the NF-kappaB activation, probably through the conversion of Tau-NHCl to NH(2)Cl. These results indicated that NH(2)Cl inhibited TNFalpha-induced NF-kappaB activation through the oxidation of IkappaB, and that NH(2)Cl is physiologically more relevant than Tau-NHCl in modifying NF-kappaB-mediated cellular responses.

Chloramines↗
PubMed2006

Establishment and evaluation of 2 monoclonal antibodies against oxidized apolipoprotein A-I (apoA-I) and its application to determine blood oxidized apoA-I levels.

BACKGROUND: Apolipoprotein A-I (apoA-I) is the major lipoprotein component of high-density lipoprotein(HDL), and plays an important role in reverse cholesterol transport. Its function is known to be influenced by oxidation. METHODS: Using H2O2-or chloramine T-oxidized apoA-I as antigen, we prepared 2 kinds of monoclonal antibodies, and established an ELISA system for the measurement of oxidized apoA-I. RESULTS: The 2 monoclonal antibodies obtained, 7D3 and 98A7, exhibited different reactivity characteristics. The serum level of oxidized apoA-I was higher in patients with either inflammatory disease or diabetes than in healthy individuals, and suggested a diversity of oxidized apoA-I. CONCLUSION: The 2 monoclonal antibodies are useful for the determination of oxidized apoA-I and study of diverse oxidized HDLs.

Adult↗
PubMed2006

N-Chlorotaurine and ammonium chloride: an antiseptic preparation with strong bactericidal activity.

The bactericidal activity of the endogenous antiseptic N-chlorotaurine (NCT) is significantly enhanced in the presence of ammonium chloride which induces the formation of monochloramine (NH(2)Cl) whose strong bactericidal activity is well known. In this study the properties of NCT plus ammonium chloride have been investigated. The reaction of active chlorine compounds like chloramine-T (N-chlorotoluene-sulfonamide sodium), chloroisocyanuric acid derivatives, hypochlorites (NaOCl, CaOCl(2)) with ammonium chloride did not stop at the stage of monochloramine, and the pungent smelling by-products di- and trichloramine, NHCl(2) and NCl(3), were also formed. This was not the case with NCT where only monochloramine was generated. The equilibrium constant of the reaction of NCT with ammonium was found to be [Formula: see text] , which allows to estimate the equilibrium concentration of monochloramine in aqueous solutions of NCT and ammonium chloride. At concentrations each ranging between 0.01% and 1.0% it comes to [NH(2)Cl]=3.5-254 ppm. As an unexpected result the monochloramine containing formulation turned out to be most stable in plain water without buffer additives. Quantitative killing assays revealed complete inactivation of 10(6) to 10(7)CFU/mL of seven bacterial strains by 0.1% NCT plus 0.1% ammonium chloride within 5 min, while with plain 0.1% NCT an incubation time of 2-4h was needed to achieve the same effect. The highly significant increase of bactericidal activity (200-300-fold) could be assigned to the presence of monochloramine which could be isolated by vacuum distillation. Aqueous solutions of NCT and ammonium chloride provide a highly effective and well tolerable antiseptic preparation appropriate to a treatment cycle of at least 1 month if stored in the refrigerator.

Ammonium Chloride↗
PubMed2005

Optimization and validation of a colorimetric assay for Tetrahymena sp. survival.

A colorimetric assay based on the reduction of 3-(4,5-dimethyl-2-thiazol-2-yl)-2,5-diphenyl-2h-tetrazolium bromide (MTT), for the quantification of Tetrahymena sp. survival is described. An increase in the concentration of Tetrahymena sp. cells from 0 to 1 x 10(6) cells/ml produced a linear (R(2)=0.9965) increase in the optical density (OD, 570-630 nm), and dead cells (pre-exposed to 250 mg/l formalin for 4 h) did not produce a background reading. Cells exposed to sublethal concentrations to formalin (100 mg/l or less for 4 h) recovered their growth. Using the MTT assay, we determined that Tetrahymena sp. is sensitive to formalin, chloramine-T, hydrogen peroxide, copper sulfate and NaCl. The sensitivity increased with increasing chemical concentrations and exposure time. Tetrahymena sp. was resistant to bromex and malachite green. The use of this assay in drug screening for the development of treatments for tetrahymenosis and as a bioassay to evaluate the toxicity of environmental toxicants is discussed.

Animals↗
PubMed2005

Synthesis of some new steroidal [16alpha,17alpha-d]-isoxazolines.

Regioselective synthesis of novel steroidal anti-inflammatory ante drug analogues, viz., [16alpha,17alpha-d]-isoxazolines 1(a-h) and 2(a-h) prepared in a single step in good yield by the reaction of 16-dehydropregnenolone acetate (16-DPA) 1 or related 21-chloro-20-oxopregnane 2 with various aldoximes (a-h) in presence of chloramine-T in refluxing ethanol.

Anti-Inflammatory Agents↗
PubMed1975

Radiolabeling of antigens: procedures and assessment of properties.

The role of labeled tracers in radioimmunoassay procedures (RIA) and the advantages of the iodine-labeled antigens over 14C or tritium-labeled antigens are discussed. Different methods of labeling with iodine isotopes are presented. The ease with which microgram amounts of hormonal proteins are tagged, achieving high specific activity with the chloramine-T procedure of Hunter and Greenwood, is indicated in a detailed presentation of a typical procedure. More sophisticated methods that present none of the drawbacks of the chemical oxidation methods for iodination would seem to have greater versatility, resulting in labeled antigens with better immunologic properties. These are likely to come into vogue for many inhouse preparations of labeled antigens in the next few years. The iodination procedures developed for haptenic substances have extended the usefulness of the RIA method to many steroidal hormones and have helped to achieve a limit of detectability at picogram levels. Greater specificity has also resulted. The assessment of the properties of the labeled antigens is equally important, and methods to evaluate the parameters of purity, immunoreactivity, specific activity as well as storage, are discussed. This review is intended to serve as an introduction to the radiolabeling of antigens or haptens. A thorough appreciation of the problems and pitfalls in these procedures is essential for the development of a new RIA or adaptation of a well-studied method for routine use.

Angiotensin II↗
PubMed2000

Prophylaxis against lipopolysaccharide-induced lung injuries by liposome-entrapped dexamethasone in rats.

Lipopolysaccharide (LPS), a component of the cell wall of Gram-negative bacteria, stimulates phagocytes to generate metabolites that play an important role in the pathogenesis of acute lung injury. In this study, the prophylactic effect of liposome-entrapped dexamethasone (L-DEX) was evaluated in an animal acute lung injury model. Rats were pretreated intratracheally with L-DEX or dexamethasone phosphate (DEX) at a dose of 800 microg dexamethasone/kg body weight; 1 hr later, pretreated animals were challenged i.v. with LPS (Escherichia coli 0111:B4, 1 mg/kg body weight) and killed 24 hr later. Challenge of saline-pretreated animals with LPS resulted in lung injury, as evidenced by increases in wet lung weight and decreases in lung angiotensin-converting enzyme and alkaline phosphatase activities, injury markers of pulmonary capillary endothelial and alveolar type II epithelial cells, respectively. Also, LPS injection resulted in significant increases in plasma phospholipase A(2), thromboxane B(2), and leukotriene B(4) concentrations. The LPS challenge also increased pulmonary myeloperoxidase and elastase activities as well as chloramine concentrations, suggestive of neutrophil infiltration and activation of the inflammatory response. Pretreatment of animals with L-DEX was significantly more effective than pretreatment with the free drug in reducing lung inflammation and other lung injuries, as indicated by the appropriate injury markers used in this study. Our results suggested that the pulmonary delivery of liposome-entrapped anti-inflammatory drugs such as dexamethasone improves prophylactic efficacy in counteracting LPS-induced lung injury.

Alkaline Phosphatase↗
PubMed2002

Inactivation and pharmacological properties of sqKv1A homotetramers in Xenopus oocytes cannot account for behavior of the squid "delayed rectifier" K(+) conductance.

Considerable published evidence suggests that alpha-subunits of the cloned channel sqKv1A compose the "delayed rectifier" in the squid giant axon system, but discrepancies regarding inactivation properties of cloned versus native channels exist. In this paper we define the mechanism of inactivation for sqKv1A channels in Xenopus oocytes to investigate these and other discrepancies. Inactivation of sqKv1A in Xenopus oocytes was found to be unaffected by genetic truncation of the N-terminus, but highly sensitive to certain amino acid substitutions around the external mouth of the pore. External TEA and K(+) ions slowed inactivation of sqKv1A channels in oocytes, and chloramine T (Chl-T) accelerated inactivation. These features are all consistent with a C-type inactivation mechanism as defined for Shaker B channels. Treatment of native channels in giant fiber lobe neurons with TEA or high K(+) does not slow inactivation, nor does Chl-T accelerate it. Pharmacological differences between the two channel types were also found for 4-aminopyridine (4AP). SqKv1A's affinity for 4AP was poor at rest and increased after activation, whereas 4AP block occurred much more readily at rest with native channels than when they were activated. These results suggest that important structural differences between sqKv1A homotetramers and native squid channels are likely to exist around the external and internal mouths of the pore.

4-Aminopyridine↗
PubMed1984

Modification of sodium channel inactivation in single myelinated nerve fibers by methionine-reactive chemicals.

Several methionine-reactive reagents, including N-bromoacetamide, N-bromosuccinimide, chloramine-T, and N-chlorosuccinimide, irreversibly slowed and prevented Na channel inactivation in single myelinated nerve fibers, whereas sulfhydryl- or tyrosine-modifying reagents had little effect. The activation process was not modified by the reagents that altered inactivation and could be modulated normally by Ca++ ions and Centruroides scorpion toxin II alpha. These results suggest that externally applied N-bromoacetamide and its related compounds specifically affect Na channel inactivation by modifying methionine residues of the channel.

Acetamides↗
PubMed1997

A mutation in segment I-S6 alters slow inactivation of sodium channels.

Slow inactivation occurs in voltage-gated Na+ channels when the membrane is depolarized for several seconds, whereas fast inactivation takes place rapidly within a few milliseconds. Unlike fast inactivation, the molecular entity that governs the slow inactivation of Na+ channels has not been as well defined. Some regions of Na+ channels, such as mu1-W402C and mu1-T698M, have been reported to affect slow inactivation. A mutation in segment I-S6 of mu1 Na+ channels, N434A, shifts the voltage dependence of activation and fast inactivation toward the depolarizing direction. The mutant Na+ current at +50 mV is diminished by 60-80% during repetitive stimulation at 5 Hz, resulting in a profound use-dependent phenomenon. This mutant phenotype is due to the enhancement of slow inactivation, which develops faster than that of wild-type channels (tau = 0.46 +/- 0.01 s versus 2.11 +/- 0.10 s at +30 mV, n = 9). An oxidant, chloramine-T, abolishes fast inactivation and yet greatly accelerates slow inactivation in both mutant and wild-type channels (tau = 0.21 +/- 0.02 s and 0.67 +/- 0.05 s, respectively, n = 6). These findings together demonstrate that N434 of mu1 Na+ channels is also critical for slow inactivation. We propose that this slow form of Na+ channel inactivation is analogous to the "C-type" inactivation in Shaker K+ channels.

Amino Acid Sequence↗
PubMed2002

Evaluation of oxidized alpha-1-antitrypsin in blood as an oxidative stress marker using anti-oxidative alpha1-AT monoclonal antibody.

BACKGROUND: alpha1-AT is a 52-kDa acute-phase protein and a typical serine proteinase inhibitor, which is present in human serum. In vivo, the inhibitor prevents tissue damage by inactivating proteinases, such as elastase, that are released from activated neutrophils in the presence of inflammation. METHODS: We obtained a monoclonal antibody against oxidized alpha1-AT(3F4) using chloramine T-oxidized alpha1-AT as the antigen. RESULTS: This antibody did not react with either the native alpha1-AT or the elastase-alpha1-AT complex. However, it reacted with alpha1-AT oxidized by various oxidants and peroxide lipid. The oxidized alpha1-AT is a polymer with a molecular mass of 100-200 kDa in addition to the 52-kDa protein that corresponds to the native alpha1-AT in sera. In vitro evaluations reveal that fatty acids are involved in the polymerization. Furthermore, the concentrations of oxidized alpha1-AT in the sera of patients with inflammatory and rheumatoid diseases were higher than those in healthy subjects. CONCLUSIONS: We considered that 3F4 is an effective antibody that can specifically recognize oxidized alpha1-AT, a marker of oxidative stress.

Animals↗
PubMed2001

Hypochlorite induces the formation of LDL(-), a potentially atherogenic low density lipoprotein subspecies.

Oxidation of low density lipoprotein (LDL) induced by hypochlorous acid (HOCl) leading to LDL(-), a minimally oxidized subspecies of LDL, was investigated. LDL(-) is characterized by its greater electronegativity and oxidative status, and is found in plasma in vivo. Its concentration was found to be elevated under conditions that predispose humans to atherosclerosis. We found that HOCl also converts LDL rapidly to an even more oxidized state, identified as LDL(2-), which is more electronegative than LDL(-). After milder oxidation for short durations, formation of LDL(-) takes place while less LDL(2-) is formed. Under these conditions, addition of methionine not only suppressed further oxidation of LDL but also favored the formation of LDL(-) over LDL(2-), possibly by removing chloramines at lysyl residues of LDL. The presence of lipoprotein-deficient plasma did not prevent HOCl-mediated conversion of LDL to more electronegative species. It is concluded that the HOCl-mediated conversion of LDL into more electronegative species might be physiologically relevant.

Arteriosclerosis↗
PubMed1999

Redox agents regulate ion channel activity in vacuoles from higher plant cells.

The ability of redox agents to modulate certain characteristics of voltage- and calcium-activated channels has been recently investigated in a variety of animal cells. We report here the first evidence that redox agents regulate the activation of ion channels in the tonoplast of higher plants. Using the patch-clamp technique, we have demonstrated that, in tonoplasts from the leaves of the marine seagrass Posidonia oceanica and the root of the sugar beet, a variety of sulphydryl reducing agents, added at the cytoplasmic side of the vacuole, reversibly favoured the activation of the voltage-dependent slow vacuolar (SV) channel. Antioxidants, like dithiothreitol (DTT) and the reduced form of glutathione, gave a reversible increase of the voltage-activated current and faster kinetics of channel activation. Other reducing agents, such as ascorbic acid, also increased the SV currents, although to a lesser extent in comparison with DTT and glutathione, while the oxidising agent chloramine-T irreversibly abolished the activity of the channel. Single channel experiments demonstrated that DTT reversibly increased the open probability of the channel, leaving the conductance unaltered. The regulation of channel activation by glutathione may correlate ion transport with other crucial mechanisms that in plants control turgor regulation, response to oxidative stresses, detoxification and resistance to heavy metals.

Ascorbic Acid↗
PubMed1987

The effect of cyclohexene, a preservative in dichloromethane on the liquid-liquid extraction and analysis of chlorinated drinking water.

Liquid-liquid extraction with dichloromethane is the Environmental Protection Agency's (EPA) method of choice for the analysis of acid or base neutral organic chemicals in water. Free radical chlorination and oxidation products of cyclohexene (the solvent preservative) in dichloromethane have been observed in extracts of chlorinated drinking water (after 10(5) fold concentration) by gas chromatography and gas chromatography-mass spectrometry. The chlorinated cyclohexene derivatives limit the quantitative and qualitative analysis of compounds eluting at Kovát's index less than 700-1000 and the use of these extracts for organoleptic and mutagenic studies. The effect of residual free chlorine in water on the cyclohexene present in the solvent was studied. Over ten cyclohexene derivatives were produced in every case when any residual free chlorine was present in the water. When chlorine is reduced to chloramine, the cyclohexene derivatives were greatly reduced in number and amount.

Chloramines↗
PubMed2001

Mode of failure in the dentin-adhesive resin-resin composite bonded joint as determined by strength-based (muTBS) and fracture-based (CNSB) mechanical testing.

OBJECTIVE: To determine the failure mode between dentin-adhesive resin-resin composite bonded joint produced with a chevron-notch short-bar (CNSB) and microtensile test methods. METHODS: Forty teeth were randomly selected for microtensile and forty for CNSB specimen fabrication and stored in 0.5% chloramine T at 37 degrees C until respective static load to failure testing at 30 and 180days. Failure modes were categorized by SEM and tested with Fisher's exact test. Within respective mechanical testing methods the probability of failure curve distributions being significantly different were analyzed by the Wald chi-square statistic. RESULTS: The characteristic fracture toughness at 30- and 180-day storage was 0.82 and 0.87MPam(1/2), while the Weibull Modulus (m) for the failure distributions, was 4.60 and 4.56, respectively. No significant difference was demonstrated in the failure distributions between these groups (p=0.45). The characteristic tensile strength (muTBS(o)) at 30- and 180-day storage was 52.53 and 14.71MPa with an m of 3.04 and 1.56, respectively. Failure distributions for muTBS groups were significantly different (p<0.001). K(IvM) failure modes, regardless of storage time, were within the adhesive joint with 30-day debonds primarily through the top region of the hybrid layer (THL) and after 180-days involving the bottom of the hybrid layer (BHL). The 30-day muTBS group demonstrated a propensity to debond in dentin or resin composite substrates but after 180-days storage debonds again involved the BHL. SIGNIFICANCE: The weak links in the dentin-adhesive resin-resin composite bonded joint may be the interphase regions between the THL and the adhesive resin and the BHL and dentin.

Adhesiveness↗
PubMed1999

Effect of monochloramine disinfection of municipal drinking water on risk of nosocomial Legionnaires' disease.

BACKGROUND: Many Legionella infections are acquired through inhalation or aspiration of drinking water. Although about 25% of municipalities in the USA use monochloramine for disinfection of drinking water, the effect of monochloramine on the occurrence of Legionnaires' disease has never been studied. METHODS: We used a case-control study to compare disinfection methods for drinking water supplied to 32 hospitals that had had outbreaks of Legionnaires' disease with the disinfection method for water supplied to 48 control-hospitals, with control for selected hospital characteristics and water treatment factors. FINDINGS: Hospitals supplied with drinking water containing free chlorine as a residual disinfectant were more likely to have a reported outbreak of Legionnaires' disease than those that used water with monochloramine as a residual disinfectant (odds ratio 10.2 [95% CI 1.4-460]). This result suggests that 90% of outbreaks associated with drinking water might not have occurred if monochloramine had been used instead of free chlorine for residual disinfection (attributable proportion 0.90 [0.29-1.00]). INTERPRETATION: The protective effect of monochloramine against legionella should be confirmed by other studies. Chloramination of drinking water may be a cost-effective method for control of Legionnaires' disease at the municipal level or in individual hospitals, and widespread implementation could prevent thousands of cases.

Case-Control Studies↗
PubMed2002

Methionine oxidation as a major cause of the functional impairment of oxidized actin.

A significant specific increase in the actin carbonyl content has been recently demonstrated in human brain regions severely affected by the Alzheimer's disease pathology, in postischemic isolated rat hearts, and in human intestinal cell monolayers following incubation with hypochlorous acid (HOCl). We have very recently shown that exposure of actin to HOCl results in the immediate loss of Cys-374 thiol, oxidation of some methionine residues, and, at higher molar ratios of oxidant to protein, increase in protein carbonyl groups, associated with filament disruption and inhibition of filament formation. In the present work, we have studied the effect of methionine oxidation induced by chloramine-T (CT), which at neutral or slightly alkaline pH oxidizes preferentially Met and Cys residues, on actin filament formation and stability utilizing actin blocked at Cys-374. Methionines at positions 44, 47, and 355, which are the most solvent-exposed methionyl residues in the actin molecule, were found to be the most susceptible to oxidation to the sulfoxide derivative. Met-176, Met-190, Met-227, and Met-269 are the other sites of the oxidative modification. The increase in fluorescence associated with the binding of 8-anilino-1-naphtalene sulfonic acid to hydrophobic regions of the protein reveals that actin surface hydrophobicity increases with oxidation, indicating changes in protein conformation. Structural alterations were confirmed by the decreased susceptibility to proteolysis and by urea denaturation curves. Oxidation of some critical methionines (those at positions 176, 190, and 269) causes a complete inhibition of actin polymerization and severely affects the stability of actin filaments, which rapidly depolymerize. The present results would indicate that the oxidation of some critical methionines disrupts specific noncovalent interactions that normally stabilize the structure of actin filaments. We suggest that the process involving formation of actin carbonyl derivatives would occur at an extent of oxidative insult higher than that causing the oxidation of some critical methionine residues. Therefore, methionine oxidation could be a damaging event preceding the appearance of carbonyl groups on actin and a major cause for the functional impairment of the carbonylated protein recently observed both in vivo and in vitro.

Actins↗