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Cetylpyridinium chloride (CPC) is an antimicrobial used in numerous personal care and janitorial products and food for human consumption at millimolar concentrations. Minimal information exists on the eukaryotic toxicology of CPC. We have investigated the effects of CPC on signal transduction of the immune cell type mast cells. Here, we show that CPC inhibits the mast cell function degranulation with antigen dose-dependence and at non-cytotoxic doses ∼1000-fold lower than concentrations in consumer products. Previously we showed that CPC disrupts phosphatidylinositol 4,5-bisphosphate, a signaling lipid critical for store-operated Ca 2+ entry (SOCE), which mediates degranulation. Our results indicate that CPC inhibits antigen-stimulated SOCE: CPC restricts Ca 2+ efflux from endoplasmic reticulum, reduces Ca 2+ uptake into mitochondria, and dampens Ca 2+ flow through plasma membrane channels. While inhibition of Ca 2+ channel function can be caused by alteration of plasma membrane potential (PMP) and cytosolic pH, CPC does not affect PMP or pH. Inhibition of SOCE is known to depress microtubule polymerization, and here we show that CPC indeed dose-dependently shuts down formation of microtubule tracks. In vitro data reveal that CPC inhibition of microtubules is not due to direct CPC interference with tubulin. In summary, CPC is a signaling toxicant that targets Ca 2+ mobilization., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier Ltd. All rights reserved.)

Quaternary ammonium compounds, including benzalkonium chloride (BAC) and cetylpyridinium chloride (CPC), are widely used as disinfectants. Increased use of inhalable products containing BAC or CPC has raised concerns for lung toxicity. This study sought to elucidate the microstructure of plasma membrane damage caused by BAC and CPC and the subsequent mechanism by which the damage is mediated, as assessed using two human pulmonary epithelial cell lines (A549 and BEAS-2B). Scanning electron microscopic observation showed that exposure to BAC or CPC for 3 hr reduced the length and density of microvilli on the plasma membrane in A549 cells. Analysis of cell cycle distribution following plasma membrane damage revealed that BAC and CPC promote G 0 /G 1 cell cycle arrest in both cell lines. The protein levels of Cdc6, an essential regulator of DNA replication during G 1 /S transition, are decreased significantly and dose dependently by BAC or CPC exposure. CPC and BAC decreased the Cdc6 levels that had been increased by a PI3K agonist in A549 cells, and levels of phosphorylated AKT were reduced in response to BAC or CPC. Conversely, exposure to equivalent concentrations of pyridinium chloride (lacking a hydrocarbon tail) induce no changes. These results suggest that plasma membrane damage triggered by BAC or CPC causes Cdc6-dependent G 0 /G 1 cell cycle arrest in pulmonary cells. These effects are attributable to the long alkyl chains of BAC and CPC. The reduction of Cdc6 following plasma membrane damage may be caused, at least in part, by diminished signaling via the PI3K/AKT pathway.

Previously, we reported on the surfactant cetylpyridinium chloride (CPC) as a crosslinker of alginate for the formation of stable polyelectrolyte-surfactant-complex nanoparticles. Here, we evaluate this system for increased solubility of a poorly soluble drug. The aim was to use CPC for solubilisation of ibuprofen and to use the micellar associates formed for alginate complexation and nanoparticle formation. We acquired deeper insights into the entropy led interactions between alginate, CPC and ibuprofen. Stable nanoparticles were formed across limited surfactant-to-polyelectrolyte molar ratios, with ~150 nm hydrodynamic diameter, monodispersed distribution, and negative zeta potential (-40 mV), with 34% ibuprofen loading. Their structure was obtained using small-angle X-ray scattering, which indicated disordered micellar associates when ibuprofen was incorporated. This resulted in nanoparticles with a complex nanostructured composition, as shown by transmission electron microscopy. Drug release from ibuprofen-cetylpyridinium-alginate nanoparticles was not hindered by alginate, and was similar to the release kinetics from ibuprofen-CPC solubilisates. These innovative carriers developed as polyelectrolyte-surfactant complexes can be used for solubilisation of poorly soluble drugs, where the surfactant simultaneously increases the solubility of the drug at concentrations below its critical micellar concentration and crosslinks the polyelectrolyte to form nanoparticles., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020 Elsevier B.V. All rights reserved.)

Biodegradability studies for the cationic surfactant cetylpyridinium chloride (CPC) are hampered by inhibitory effects on inoculum at prescribed test concentrations (10-20 mg organic carbon/L). In this study, we used 14 C labeled CPC in the 28 d Headspace Test (OECD 310) and demonstrated that CPC was readily biodegradable (10->60% mineralization within a 10 day window) at test concentrations 0.006-0.3 mg/L with CPC as single substrate. Biodegradation efficiency was comparable over this concentration range. CPC inhibited degradation at 1 mg/L and completely suppressed inoculum activity at 3 mg/L. In an extensive sorbent modified biodegradation study we evaluated the balance between CPC bioaccessibility and toxicity. A non-inhibitory concentration of 0.1 mg/L CPC was readily biodegradable with 83% sorbed to SiO 2 , while biodegradation was slower when 96% was sorbed. SiO 2 mitigated inhibitory effects of 1 mg/L CPC, reaching >60% biodegradation within 28 d; inhibitory effects were also mitigated by addition of commercial clay powder (illite) but this was primarily reflected by a reduced lag phase. At 10 mg/L CPC SiO 2 was still able to mitigate inhibitory effects, but bioaccessibility seemed limited as only 20% biodegradation was reached. Illite limited bioaccessibility more strongly and was not able to sustain biodegradation at 10 mg/L CPC., (Copyright © 2019 Elsevier Inc. All rights reserved.)

Hepatitis B virus (HBV) infection is a major risk factor for chronic liver disease, cirrhosis, and hepatocellular carcinoma (HCC) worldwide. While multiple hepatitis B drugs have been developed, build up of drug resistance during treatment or weak efficacies observed in some cases have limited their application. Therefore, there is an urgent need to develop substitutional pharmacological agents for HBV-infected individuals. Here, we identified cetylpyridinium chloride (CPC) as a novel inhibitor of HBV. Using computational docking of CPC to core protein, microscale thermophoresis analysis of CPC binding to viral nucleocapsids, and in vitro nucleocapsid formation assays, we found that CPC interacts with dimeric viral nucleocapsid protein (known as core protein or HBcAg) specifically. Compared with other HBV inhibitors, such as benzenesulfonamide (BS) and sulfanilamide (SA), CPC achieved significantly better reduction of HBV particle number in HepG2.2.15 cell line, a derivative of human HCC cells that stably expresses HBV. CPC also inhibited HBV replication in mouse hydrodynamic model system. Taken together, our results show that CPC inhibits capsid assembly and leads to reduced HBV biogenesis. Thus, CPC is an effective pharmacological agent that can reduce HBV particles., (Copyright © 2019 Elsevier B.V. All rights reserved.)

Our lab has previously shown that nitric oxide (NO) can alter the synaptic response properties of amacrine cells by releasing Cl- from internal acidic compartments. This alteration in the Cl- gradient brings about a positive shift in the reversal potential of the GABA-gated current, which can convert inhibitory synapses into excitatory synapses. Recently, we have shown that the cystic fibrosis transmembrane regulator (CFTR) Cl- channel is involved in the Cl- release. Here, we test the hypothesis that (acidic) synaptic vesicles are a source of NO-releasable Cl- in chick retinal amacrine cells. If SVs are a source of Cl-, then depleting synaptic vesicles should decrease the nitric oxide-dependent shift in the reversal potential of the GABA-gated current. The efficacy of four inhibitors of dynamin (dynasore, Dyngo 4a, Dynole 34-2, and MiTMAB) were evaluated. In order to deplete synaptic vesicles, voltage-steps were used to activate V-gated Ca2+ channels and stimulate the synaptic vesicle cycle either under control conditions or after treatment with the dynamin inhibitors. Voltage-ramps were used to measure the NO-dependent shift in the reversal potential of the GABA-gated currents under both conditions. Our results reveal that activating the synaptic vesicle cycle in the presence of dynasore or Dyngo 4a blocked the NO-dependent shift in EGABA. However, we also discovered that some dynamin inhibitors reduced Ca2+ signaling and L-type Ca2+ currents. Conversely, dynasore also increased neurotransmitter release at autaptic sites. To further resolve the mechanism underlying the inhibition of the NO-dependent shift in the reversal potential for the GABA-gated currents, we also tested the effects of the clathrin assembly inhibitor Pitstop 2 and found that this compound also inhibited the shift. These data provide evidence that dynamin inhibitors have multiple effects on amacrine cell synaptic transmission. These data also suggest that inhibition of endocytosis disrupts the ability of NO to elicit Cl- release from internal stores which may in part be due to depletion of synaptic vesicles., Competing Interests: The authors have declared that no competing interests exist.

Apolipoprotein L1 (ApoL1) is a human serum protein conferring resistance to African trypanosomes, and certain ApoL1 variants increase susceptibility to some progressive kidney diseases. ApoL1 has been hypothesized to function like a pore-forming colicin and has been reported to have permeability effects on both intracellular and plasma membranes. Here, to gain insight into how ApoL1 may function in vivo , we used vesicle-based ion permeability, direct membrane association, and intrinsic fluorescence to study the activities of purified recombinant ApoL1. We found that ApoL1 confers chloride-selective permeability to preformed phospholipid vesicles and that this selectivity is strongly pH-sensitive, with maximal activity at pH 5 and little activity above pH 7. When ApoL1 and lipid were allowed to interact at low pH and were then brought to neutral pH, chloride permeability was suppressed, and potassium permeability was activated. Both chloride and potassium permeability linearly correlated with the mass of ApoL1 in the reaction mixture, and both exhibited lipid selectivity, requiring the presence of negatively charged lipids for activity. Potassium, but not chloride, permease activity required the presence of calcium ions in both the association and activation steps. Direct assessment of ApoL1-lipid associations confirmed that ApoL1 stably associates with phospholipid vesicles, requiring low pH and the presence of negatively charged phospholipids for maximal binding. Intrinsic fluorescence of ApoL1 supported the presence of a significant structural transition when ApoL1 is mixed with lipids at low pH. This pH-switchable ion-selective permeability may explain the different effects of ApoL1 reported in intracellular and plasma membrane environments., (© 2017 by The American Society for Biochemistry and Molecular Biology, Inc.)

The potential damage of Alzheimer's disease (AD) in brain function has attracted extensive attention. As the most common anion, Cl - has been indicated to play significant roles in brain diseases, particularly in the pathological process of AD. In this work, a label-free selective and accurate electrochemical biosensor was first developed for real-time monitoring of Cl - levels in a mouse brain model of AD and rat brain upon global cerebral ischemia. Silver nanoparticles (AgNPs) were designed and synthesized as selective recognition element for Cl - , while 5'-MB-GGCGCGATTTT-SH-3' (SH-DNA-MB, MB = methylene blue) was selected as an inner reference molecule for a built-in correction to avoid the effects from the complicated brain. The electrochemical biosensor showed high accuracy and remarkable selectivity for determination of Cl - over other anions, metal ions, amino acids, and other biomolecules. Furthermore, three-dimensional nanostructures composed of single-walled carbon nanotubes (SWNTs) and Au nanoleaves were assembled on the carbon fiber microelectrode (CFME) surface to enhance the response signal. Finally, the developed biosensor with high analytical performance, as well as the unique characteristic of CFME itself including inertness in live brain and good biocompatibility, was successfully applied to in vivo determination of Cl - levels in three brain regions: striatum, hippocampus, and cortex of live mouse and rat brains. The comparison of average levels of Cl - in normal striatum, hippocampus, and cortex of normal mouse brains and those in the mouse model brains of AD was reported. In addition, the results in rat brains followed by cerebral ischemia demonstrated that the concentrations of Cl - decreased by 19.8 ± 0.5% (n = 5) in the striatum and 27.2 ± 0.3% (n = 5) in hippocampus after cerebral ischemia for 30 min, but that negligible change in Cl - concentration was observed in cortex.

Using patch-clamp method (whole cell configuration), it was shown that tetraethylammonium (TEA) and 4-aminopyridine (4-AP) block calcium-dependent chloride currents in the membrane of freshly isolated cerebellar Purkinje cells of rats (12-15 days). In the concentration range studied (50 μM-10 mM TEA and 100 μM-1 mM 4-AP), both compounds blocked the chloride current at IC 50 130 μM for TEA and 110 μM for 4-AP. TEA blockade was reversible after washing. The effect of 4-AP at concentrations greater than 100 μM was irreversible: both outward and inward chloride currents were blocked even after the removal of 4-AP from the incubation medium.

Salinity tolerance is correlated with shoot chloride (Cl(-)) exclusion in multiple crops, but the molecular mechanisms of long-distance Cl(-) transport are poorly defined. Here, we characterize the in planta role of AtSLAH1 (a homologue of the slow type anion channel-associated 1 (SLAC1)). This protein, localized to the plasma membrane of root stelar cells, has its expression reduced by salt or ABA, which are key predictions for a protein involved with loading Cl(-) into the root xylem. Artificial microRNA knockdown mutants of AtSLAH1 had significantly reduced shoot Cl(-) accumulation when grown under low Cl(-), whereas shoot Cl(-) increased and the shoot nitrate/chloride ratio decreased following AtSLAH1 constitutive or stelar-specific overexpression when grown in high Cl(-) In both sets of overexpression lines a significant reduction in shoot biomass over the null segregants was observed under high Cl(-) supply, but not low Cl(-) supply. Further in planta data showed AtSLAH3 overexpression increased the shoot nitrate/chloride ratio, consistent with AtSLAH3 favouring nitrate transport. Heterologous expression of AtSLAH1 in Xenopus laevis oocytes led to no detectible transport, suggesting the need for post-translational modifications for AtSLAH1 to be active. Our in planta data are consistent with AtSLAH1 having a role in controlling root-to-shoot Cl(-) transport., (© The Author 2016. Published by Oxford University Press on behalf of the Society for Experimental Biology.)

Objective: Halitosis is a common complaint affecting the majority of the population. Mouthrinses containing cetylpyridinium chloride (CPC) have been used as oral hygiene aids to suppress oral malodor. Although the clinical efficacy of these mouthrinses has been well-documented, the mechanism whereby CPC reduces malodor is less-well-understood. We hypothesized that CPC suppresses expression of the genes (mgl and cdl) and enzymes responsible for methyl mercaptan (CH3SH) and hydrogen sulfide (H2S) production by oral anaerobes associated with halitosis. In this study, the mgl and cdl expression of Porphyromonas gingivalis and Fusobacterium nucleatum in the presence of CPC was investigated., Materials and Methods: We used a microdilution method to determine the growth and production of volatile sulfur compounds (VSCs) by P. gingivalis W83 and F. nucleatum ATCC 10953 in respective media containing CPC (0.5 μg/mL to 1.5 μg/mL). For metabolic activity, we used an XTT {2,3-bis(2-methyloxy-4-nitro-5-sulfophenyl)-2H-tetrazolium-5-carboxanilide} reduction assay. We used real-time RT-PCR and Western blotting to evaluate the effect of CPC at sub-MIC levels on mgl and cdl expression at the transcriptional and enzymatic levels., Results: CPC inhibited the growth of P. gingivalis and F. nucleatum at MICs of 3 μg/mL and 2 μg/mL, and at MBCs of 6 μg/mL and 3 μg/mL, respectively. Compared with untreated controls, CPC at 1.5 μg/mL suppressed CH3SH production of P. gingivalis by 69.84%±2.88% and H2S production of F. nucleatum by 82.55%±8.36% (p<0.05) without affecting metabolic activity. Inhibition of mgl mRNA (81.58%±20.33%) and protein (39.15%±6.65%) expression in P. gingivalis and inhibition of cdl mRNA (61.76%±13.75%) and protein (64.34%±1.62%) expression in F. nucleatum were also noted (p<0.05)., Conclusion: CPC represents an effective agent for halitosis reduction by inhibiting the growth and suppressing the expression of specific genes related to VSC production in anaerobic periodontal pathogens., (Published by Elsevier Ltd.)

The main objective of this work was to investigate the biosorption performance of unmodified and Cetylpyridinium chloride (CPC)-modified biomass of Penicillium YW 01 for Acid Blue 25 (AB 25). Maximum biosorption capacity of AB 25 onto CPC-modified biosorbent was 118.48 mg g(-1) under phosphoric-phosphate buffer with initial dye concentration of 200 mg L(-1) at 30°C. The biosorption pattern of AB 25 onto unmodified biosorbent in aqueous solution and phosphoric-phosphate buffer was well fitted with both Langmuir and Freundlich isotherm models. While the equilibrium data of CPC-modified biosorbent in aqueous solution and phosphoric-phosphate buffer failed to fit the Freundlich isotherm model, indicating the monolayer biosorption formed onto CPC-modified biosorbent. The values of initial biosorption rate of biosorbent in phosphoric-phosphate buffer were found to be higher than that of corresponding values in aqueous solution, indicating phosphoric-phosphate buffer enhanced the initial biosorption rate of biosorption process. Weber-Morris model analysis indicated that the boundary layer effect had more influence on the biosorption process in phosphoric-phosphate buffer. The BET surface area of CPC-modified biosorbent (0.5761 m(2) g(-1)) was larger than that of unmodified biomass (0.3081 m(2) g(-1)). Possible dye-biosorbent interactions were confirmed by Fourier transform infrared spectroscopy., (Copyright © 2011 Elsevier B.V. All rights reserved.)

A new method for the determination of tea polysaccharide (TPS) in green tea (Camellia sinensis) leaves has been developed. The method was based on the enhancement of resonance light scattering (RLS) of TPS in the presence of cetylpyridinium chloride (CPC)-NaOH system. Under the optimum conditions, the RLS intensity of CPC was greatly enhanced by adding TPS. The maximum peak of the enhanced RLS spectra was located at 484.02 nm. The enhanced RLS intensity was proportional to the concentration of TPS in the range of 2.0-20 μg/ml. It showed that the new method and phenol-sulfuric acid method give some equivalent results by measuring the standard compounds. The recoveries of the two methods were 96.39-103.7% (novel method) and 100.15-103.65% (phenol-sulfuric acid method), respectively. However, it showed that the two methods were different to some extent. The new method offered a limit of detection (LOD) of 0.047 μg/ml, whereas the phenol-sulfuric acid method gives a LOD of 1.54 μg/ml. Interfered experiment demonstrated that the new method had highly selectivity, and was more suitable for the determination of TPS than phenol-sulfuric method. Stability test showed that new method had good stability. Moreover, the proposed method owns the advantages of easy operation, rapidity and practicability, which suggested that the proposed method could be satisfactorily applied to the determination of TPS in green tea., (Copyright © 2011 Elsevier B.V. All rights reserved.)

The aim of this study was to determine the contribution of plaque and saliva towards the prolonged activity, also called substantivity, of three antimicrobial mouthrinses (Listerine®, Meridol®, Crest Pro Health®), used in combination with a toothpaste (Prodent Coolmint®). Volunteers brushed for 4 weeks with a toothpaste without antimicrobial claims, while during the last 2 weeks half of the volunteers used an antimicrobial mouthrinse in addition to brushing. At the end of the experimental period, plaque and saliva samples were collected 6 h after oral hygiene, and bacterial concentrations and viabilities were determined. The contribution of plaque and saliva towards substantivity was assessed by combining plaque obtained after mechanical cleaning only with plaque and saliva obtained after additional use of an antimicrobial rinse. Subsequently, resulting viabilities of the combined plaques were determined. The viabilities of plaque samples after additional rinsing with mouthrinses were lower than of plaque obtained after mechanical cleaning only, regardless of the rinse involved. Moreover, plaque collected 6 h after rinsing with antimicrobial mouthrinses contained a surplus of antimicrobial activity. Only Listerine showed decreased viability in saliva, but none of the mouthrinses showed any residual antimicrobial activity in saliva. The findings indicate that plaque left behind after mechanical cleaning contributes to the prolonged substantivity of antimicrobial mouthrinses., (Copyright © 2010 S. Karger AG, Basel.)

Biofilms are composed of bacterial cells encased in a self-synthesized, extracellular polymeric matrix. Poly-beta(1,6)-N-acetyl-d-glucosamine (PNAG) is a major biofilm matrix component in phylogenetically diverse bacteria. In this study we investigated the physical and chemical properties of the PNAG matrix in biofilms produced in vitro by the gram-negative porcine respiratory pathogen Actinobacillus pleuropneumoniae and the gram-positive device-associated pathogen Staphylococcus epidermidis. The effect of PNAG on bulk fluid flow was determined by measuring the rate of fluid convection through biofilms cultured in centrifugal filter devices. The rate of fluid convection was significantly higher in biofilms cultured in the presence of the PNAG-degrading enzyme dispersin B than in biofilms cultured without the enzyme, indicating that PNAG decreases bulk fluid flow. PNAG also blocked transport of the quaternary ammonium compound cetylpyridinium chloride (CPC) through the biofilms. Binding of CPC to biofilms further impeded fluid convection and blocked transport of the azo dye Allura red. Bioactive CPC was efficiently eluted from biofilms by treatment with 1 M sodium chloride. Taken together, these findings suggest that CPC reacts directly with the PNAG matrix and alters its physical and chemical properties. Our results indicate that PNAG plays an important role in controlling the physiological state of biofilms and may contribute to additional biofilm-associated processes such as biocide resistance.

Objectives: Cetylpyridinium chloride (CPC), a quaternary ammonium compound, was shown to interact irreversibly with Streptococcus mutans biofilms, leading to a slow diffusion compared with poly(ethylene glycol) (PEG) molecules of similar size. The objective of this work is to determine if the retardation of CPC diffusion and its strong binding to biofilms is caused by interactions between the ammonium group of CPC and the exopolysaccharide (EPS) matrix., Methods: First, we characterized the diffusion of two analogues of CPC in S. mutans biofilms: dodecylpyridinium chloride (DPC), carrying a shorter alkyl chain than CPC, and tetramethylene bispyridinium chloride (TMBPC), a compound carrying two positively charged ammonium groups. Second, we cultured biofilms with different densities of EPS and examined the impact of this density on the transport properties of CPC. The diffusion of these compounds was probed using infrared spectroscopy with attenuated total reflectance sampling., Results: The diffusion of CPC, DPC and TMBPC in S. mutans biofilm is slower than that of PEG10k. In addition, TMBPC and DPC, as PEG10k, could be readily washed out from the biofilms while CPC association was practically irreversible. The penetration of CPC through the EPS matrix was found to be not significantly affected by the increased EPS density, whereas the penetration of PEG with a molar mass of 10k was considerably reduced., Conclusions: These results suggest that the interactions between the quaternary ammonium groups and the EPS matrices are not the prime contribution of the strong CPC binding, and the alkyl chain length plays a role in this association, likely through hydrophobic interactions.

The binding of cetylpyridinum chloride (CPC) with glucose oxidase (GOD) has been extensively studied at various experimental conditions such as ionic strength, urea concentration and pH at 25 degrees C, using ion-selective membrane electrodes, UV-vis absorption spectroscopy and enzyme activity assay method. The accurate binding isotherms have been obtained and analyzed in terms of Scatchard plot and binding capacity concept. The results represent two binding set system for most of studied conditions. The values of Hill equation parameters have been estimated and used for calculation of intrinsic Gibbs free energy of binding. The results have been interpreted in terms of structural viewpoint of GOD and nature of interactions in the solution. The interpretations are in good agreement with denaturation experiment. Activity measurements represent the significant activation of enzyme due to binding of first CPC molecules. However, the binding of subsequent CPC diminished the activity of enzyme which may be due to the binding of second CPC to enzyme active site. The complete deactivation of enzyme is reached due to binding of about five CPC ions.

The complexation of oligonucleotides and antisense drugs with a cationic surfactant, cetylpyridinium chloride (CPC), has been studied using electrochemistry at a micrometer sized liquid/liquid interface. This method can be used to investigate the effect of chemical and structural modifications on the complexation behaviour of oligonucleotides. For the interaction between CPC and oligonucleotides the effect of phosphorothioate derivatisation upon binding characteristics has been examined. Phosphoromonothioate modification causes the onset of binding to occur at a lower free surfactant concentration. Calorimetric studies show that surfactants are strongly bound to oligonucleotides and the binding is driven by entropy. The enthalpy change for the formation of oligonucleotide-surfactant complex is negative in all cases at 25 degrees C indicating exothermic reaction.

The interaction of negatively charged liquid phosphatidylcholine/cardiolipin liposomes with water-soluble negatively charged DNA/cetylpyridinium bromide and DNA/poly(N-alkyl-4-vinylpyridinium bromide) complexes was studied. It is shown that the DNA/cetylpyridinium bromide complex while interacting with the liposomes is destroyed, so that the cetylpyridinium cation is incorporated into the liposomal membrane and DNA remains in the solution. The DNA/poly-(N-ethyl-4-vinylpyridinium bromide) complex does not interact at all with the liposomes. On the contrary, the complex of DNA with the poly(vinylpyridinium) cation carrying a small amount of N-cetyl groups is adsorbed on the membrane as a whole. The data obtained indicate that complexation of DNA with hydrophobized polycations can be used for enhancing DNA affinity to biological membranes.

Quantitation of uronic acid precipitable by cetylpyridinium chloride (CPC) and electrophoretic separation of glycosaminoglycans were performed on sera from patients with chronic renal failure and compared to normal controls. Serum CPC-precipitable uronic acid (CpUA) levels in patients with renal failure were significantly higher (mean 13.7 mg/L, range 7.1-23.6 mg/L) than normal controls (mean 9.6 mg/L, range 5.1-13.9 mg/L) due to increased concentrations of low sulphated chondroitin sulphate. A positive correlation between serum CpUA and creatinine was found in renal failure patients. Urine CpUA excretion was raised in renal failure patients compared to normal controls with an increased excretion of chondroitin sulphate (Ch-S) of reduced electrophoretic mobility. Heparan sulphate (HS), a major glycosaminoglycan in normal urine, was absent from the urine of these patients. The possible origin of urine glycosaminoglycans and the role of the kidney in glycosaminoglycan metabolism are discussed.

Studies have shown that cetylpyridinium chloride (CPC) containing mouthwash may in vitro inhibit artificial bacterial plaque accumulation under certain conditions. These studies, together with the findings of clinical trials, suggest that the clinical activity of CPC in partially limiting plaque accumulation depends on its adherence to cleaned enamel surfaces rather than its penetration in performed plaque.

A modification of the Colowick and Womack procedure for measuring ligand binding by macromolecules is described for drug binding by bacteria. This technique is based on the determination of drug concentration in the dialysate from a bacteria-drug mixture at equilibrium. The dialysis cell of the original procedure was replaced by a Minibeaker (Bio-Rad), which has a larger membrane surface area, and the dialysate was continuously monitored with a spectrophotometer equipped with a flow cell. With this system, only 3 min was required to determine the amount of cetylpyridinium chloride bound by Escherichia coli K-12 strain P678. Possible applications of the technique are discussed.