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Chemical Compound Review

Roccal     benzyl-dimethyl-tridecyl- azanium chloride

Synonyms: CHEMBL502109, AG-D-67392, CCG-39344, NSC-758480, AC1MHZ1E, ...
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Disease relevance of benzyl-dimethyl-tridecyl-azanium

  • RESULTS: Cellular viability decreased as BAC concentration increased, but it was accompanied by concentration-dependent toxicity [1].
  • An increase of at least 2-fold in distal colon wall thickness confirmed the induction of megacolon in BAC-treated rats [2].
  • Higher concentrations of the cationic agents BAC and benzethonium chloride caused a generalized tissue damage including disruption of the smooth muscle, lymphocytic infiltration, intestinal perforation and death [3].
  • None of the Enterococcus spp. from broiler, cattle, and pigs, the antibiotic-resistant E. coli from pig intestine and fish pathogens Vibrio spp. and Aeromonas spp. from the Norwegian fish farming industry were resistant to BC [4].
  • In conclusion, BC resistance among food-associated Gram-negative bacteria and Enterococcus spp. is not frequent, but resistance may develop to user concentrations after exposure to sublethal concentrations of BC [4].
 

High impact information on benzyl-dimethyl-tridecyl-azanium

  • BACKGROUND: It has been shown previously that myenteric plexus destruction by benzalkonium chloride (BAC) increased villus height, crypt depth, and muscle thickness, suggesting that these neurons influence intestinal morphology [5].
  • METHODS: Six groups of rats were studied: control, chemical denervation (3 mmol/L BAC), surgical denervation, intraluminal stasis produced by partial obstruction, chemical inflammation (5% acetic acid), and surgical inflammation (serosa removal only) [5].
  • Our goals were to (1) show that the morphological sequelae of BAC treatment are caused by myenteric plexus removal and not the factors listed above, and (2) determine whether segmental myenteric plexus removal alters morphology elsewhere in the small intestine [5].
  • Bronchoconstriction from inhaled BAC is cumulative, prolonged, and correlates directly with basal airway responsiveness [6].
  • METHODS: Corneal and conjunctival cell lines were incubated with preserved (benzalkonium chloride [BAC]) or unpreserved ofloxacin solutions for 15 minutes [7].
 

Chemical compound and disease context of benzyl-dimethyl-tridecyl-azanium

 

Biological context of benzyl-dimethyl-tridecyl-azanium

  • Moreover, the higher frequency of antibiotic resistance among BC-resistant strains indicates that the presence of either resistance determinant selects for the other during antimicrobial therapy and disinfection in hospitals [10].
  • Reactive oxygen species and superoxide anion productions observed for all solutions were significantly higher for the preserved ofloxacin and BAC solutions, which also induced apoptosis (chromatin condensation and translocation of phosphatidylserine) through P2X7 pore opening, whereas unpreserved ofloxacin did not [7].
  • BAC treatment resulted in an erratic, markedly distorted basic electric rhythm and an alteration in spike potential generation [3].
  • In the BKC low irritant-threshold group, we found a significant increase in the A allele (P=0.002) and AA genotype (P=0.016) [11].
  • The addition of F-5A gel containing 0.5% of each one of the spermicide ingredients (CA, NX9 and BZC) produced the total suppression of sperm motility within 30 s at a dilution of 1/50 [12].
 

Anatomical context of benzyl-dimethyl-tridecyl-azanium

  • Reduced reactive oxygen species production could be the main mechanism by which prostaglandin analogs protect epithelial cells from the proapoptotic effects of BAC [1].
  • Dose-response curves obtained in control and BAC-treated jejunum were nearly superimposable regardless of the beta agonist used [13].
  • Because nerve-mediated longitudinal muscle responses are lost despite the presence of an intact submucosal plexus in the BAC-treated jejunum, our data suggest that the motor neurons innervating the rat jejunal longitudinal muscle are located in the myenteric plexus [14].
  • In the current study, we measured the area of VIP neurons of submucous plexus in the ileum of weanling rats, in which myenteric neurons were ablated by serosal application of benzalkonium chloride (BAC) [15].
  • A nasal decongestant spray composed of a combination of vasoactive substances and BKC has a long-term adverse effect on the nasal mucosa [16].
 

Associations of benzyl-dimethyl-tridecyl-azanium with other chemical compounds

  • Of these chemicals, only NiCl2 and DNCB significantly increased the surface expression of CD54, CD86, HLA-DR antigen, and interleukin (IL)-1 beta production, while SDS, BC, or ZnCl2 could not augment them, except for weak augmentation of CD86 expression by SDS [17].
  • PURPOSE: In a previous study, it was demonstrated that in vitro in a human conjunctiva-derived cell line, latanoprost in its commercial presentation appeared to be less toxic than the benzalkonium chloride (BAC) it contains as a preservative [1].
  • Neuronal counts from BAC and control rats not treated with DMH showed an average denervation of 63% [2].
  • The beta adrenergic receptor agonists isoproterenol and sulfonterol produced a concentration-dependent relaxation of both control and BAC-treated jejunum [13].
  • The alpha-1 selective agonists phenylephrine and methoxamine were more potent and efficacious in producing relaxation of control than BAC-treated jejunum [13].
 

Gene context of benzyl-dimethyl-tridecyl-azanium

  • In the three other BC and penicillin-resistant strains, the qacA/B and blaZ genes were located on separate plasmids [18].
  • The irritants BA and BZC did not induce up-regulation of CD86 expression when tested at concentrations that induced similar levels of cytotoxicity [19].
  • BZC was less effective at provoking increases in this cytokine; concentrations (1%) that caused marked edema failed to stimulate significant changes in IL-6 expression [20].
  • The failure of BZC to initiate TNF-alpha production in the skin was not attributable to inhibition of the bioassay used to measure this cytokine and was apparently independent of the stimulation by this chemical of TNF-alpha inhibitory factors [20].
  • The region partially affected by BAC contained some c-kit-positive cells, and either normal or vacuolated ICC-MP were observed by electron microscopy [21].
 

Analytical, diagnostic and therapeutic context of benzyl-dimethyl-tridecyl-azanium

  • Fifteen days after treatment, both BAC-treated and untreated control jejunal segments were removed from each animal for pharmacological studies [14].
  • Short-pulse duration transmural electrical stimulation (0.1 msec) caused a frequency-dependent, tetrodotoxin-sensitive contraction in control but not BAC-treated tissues [14].
  • To address these questions, we ablated the myenteric plexus in the mouse colon with BAC and followed changes in the adjacent ICC (ICC-MP) from day 2 to day 70 after treatment, by using c-kit-immunohistochemistry and electron microscopy [21].
  • For example, a standard 2.5-mg dose of albuterol nebulizer solution contains 50 microg of BAC when administered from the multidose dropper bottle and 300 microg from the unit-dose screw-cap product [8].
  • In an attempt to overcome this problem the application of a 'Teflon' (polytetrafluoroethylene) stent and an antimicrobial benzalkonium chloride (BZC) impregnated polymer were investigated [22].

References

  1. In vitro comparison of cytoprotective and antioxidative effects of latanoprost, travoprost, and bimatoprost on conjunctiva-derived epithelial cells. Guenoun, J.M., Baudouin, C., Rat, P., Pauly, A., Warnet, J.M., Brignole-Baudouin, F. Invest. Ophthalmol. Vis. Sci. (2005) [Pubmed]
  2. The relationship between megacolon and carcinoma of the colon: an experimental approach. Garcia, S.B., Oliveira, J.S., Pinto, L.Z., Muccillo, G., Zucoloto, S. Carcinogenesis (1996) [Pubmed]
  3. Surfactants selectively ablate enteric neurons of the rat jejunum. Fox, D.A., Epstein, M.L., Bass, P. J. Pharmacol. Exp. Ther. (1983) [Pubmed]
  4. Resistance to quaternary ammonium compounds in food-related bacteria. Sidhu, M.S., Sørum, H., Holck, A. Microb. Drug Resist. (2002) [Pubmed]
  5. Myenteric plexus destruction alters morphology of rat intestine. Hadzijahic, N., Renehan, W.E., Ma, C.K., Zhang, X., Fogel, R. Gastroenterology (1993) [Pubmed]
  6. Bronchoconstrictor additives in bronchodilator solutions. Asmus, M.J., Sherman, J., Hendeles, L. J. Allergy Clin. Immunol. (1999) [Pubmed]
  7. Fluoroquinolone eye drop-induced cytotoxicity: role of preservative in P2X7 cell death receptor activation and apoptosis. Dutot, M., Pouzaud, F., Larosche, I., Brignole-Baudouin, F., Warnet, J.M., Rat, P. Invest. Ophthalmol. Vis. Sci. (2006) [Pubmed]
  8. Preservatives in nebulizer solutions: risks without benefit. Beasley, R., Fishwick, D., Miles, J.F., Hendeles, L. Pharmacotherapy (1998) [Pubmed]
  9. In vitro antiseptic susceptibility of clinical isolates from nosocomial infections. Shimizu, M., Okuzumi, K., Yoneyama, A., Kunisada, T., Araake, M., Ogawa, H., Kimura, S. Dermatology (Basel) (2002) [Pubmed]
  10. Frequency of disinfectant resistance genes and genetic linkage with beta-lactamase transposon Tn552 among clinical staphylococci. Sidhu, M.S., Heir, E., Leegaard, T., Wiger, K., Holck, A. Antimicrob. Agents Chemother. (2002) [Pubmed]
  11. Association of TNFA gene polymorphism at position -308 with susceptibility to irritant contact dermatitis. Allen, M.H., Wakelin, S.H., Holloway, D., Lisby, S., Baadsgaard, O., Barker, J.N., McFadden, J.P. Immunogenetics (2000) [Pubmed]
  12. Effects of cholic acid and 'Protectaid' formulations on human sperm motility and ultrastructure. Courtot, A.M., Nikas, G., Gravanis, A., Psychoyos, A. Hum. Reprod. (1994) [Pubmed]
  13. Ablation of the myenteric plexus impairs alpha but not beta adrenergic receptor-mediated mechanical responses of rat jejunal longitudinal muscle. Fox, D.A., Bass, P. J. Pharmacol. Exp. Ther. (1986) [Pubmed]
  14. Pharmacological characterization of rat jejunal contractility after chronic ablation of the myenteric plexus. Fox, D.A., Bass, P. J. Pharmacol. Exp. Ther. (1986) [Pubmed]
  15. Ileal VIP submucous neurons: confocal study of the area enlargement induced by myenteric denervation in weanling rats. Hernandes, L., Gama, P., Alvares, E.P. Regul. Pept. (2004) [Pubmed]
  16. Rhinitis medicamentosa: aspects of pathophysiology and treatment. Graf, P. Allergy (1997) [Pubmed]
  17. Dendritic cells differently respond to haptens and irritants by their production of cytokines and expression of co-stimulatory molecules. Aiba, S., Terunuma, A., Manome, H., Tagami, H. Eur. J. Immunol. (1997) [Pubmed]
  18. Genetic linkage between resistance to quaternary ammonium compounds and beta-lactam antibiotics in food-related Staphylococcus spp. Sidhu, M.S., Heir, E., Sørum, H., Holck, A. Microb. Drug Resist. (2001) [Pubmed]
  19. Relationship of CD86 surface marker expression and cytotoxicity on dendritic cells exposed to chemical allergen. Hulette, B.C., Ryan, C.A., Gildea, L.A., Gerberick, G.F. Toxicol. Appl. Pharmacol. (2005) [Pubmed]
  20. Differential induction of cutaneous TNF-alpha and IL-6 by topically applied chemicals. Holliday, M.R., Corsini, E., Smith, S., Basketter, D.A., Dearman, R.J., Kimber, I. Am. J. Contact Dermatitis (1997) [Pubmed]
  21. Plasticity of interstitial cells of Cajal: a study of mouse colon. Faussone-Pellegrini, M.S., Vannucchi, M.G., Ledder, O., Huang, T.Y., Hanani, M. Cell Tissue Res. (2006) [Pubmed]
  22. Role of antimicrobial-impregnated polymer and Teflon in the prevention of biliary stent blockage. Rees, E.N., Tebbs, S.E., Elliott, T.S. J. Hosp. Infect. (1998) [Pubmed]
 
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