Disease relevance of carbocysteine

• Two Glu-166 mutants of beta-lactamase I from Bacillus cereus 569/H were constructed: one with a lengthened side chain (E166Cmc, the S-carboxymethylcysteine mutant) and the other with the side chain shortened and made non-polar (E166A) [1].
• These findings suggest that carbocysteine promotes the repair of damaged epithelium by allergic reaction and may be useful in allergic airway diseases accompanied by isolated chronic coughing, especially eosinophilic bronchitis without asthma and tracheobronchitis with cough hypersensitivity [2].
• The aim of the study was to examine the effects of a mucolytic drug, carbocisteine, on rhinovirus (RV) infection in the airways [3].
• Carbocysteine therapy in older people with chronic obstructive pulmonary disease [4].
• Attachment of bacteria to human pharyngeal epithelial cells is the initial step in the pathogenesis of infection and S-carboxymethylcysteine (S-CMC) can modulate the attachment of Moraxella catarrhalis and nontypable Haemophilus influenzae to epithelial cells [5].

High impact information on carbocysteine

• Carbocisteine sulphoxidation phenotype [6].
• All other tryptic peptides, including eight peptides containing S-carboxymethylcysteine, were common in ALDH2 and CRM [7].
• To determine if a genetic polymorphism for this biotransformation pathway exists, metabolic ratios (% urinary excretion carbocisteine/% urinary excretion CMTC) for 120 healthy volunteers were assessed using high-performance thin-layer chromatography [8].
• Capillary electrophoretic determination of S-carboxymethyl-L-cysteine and its major metabolites in human urine: feasibility investigation using on-column detection of non-derivatized solutes in capillaries with minimal electroosmosis [9].
• Although carbocysteine can repair the damage of epithelial cells caused by exposure to various agents, the effects of this agent on allergic airway diseases such as asthma and eosinophilic bronchitis with an isolated chronic cough, in both of which epithelial damage may be characteristic, is not clear [2].

Chemical compound and disease context of carbocysteine

• Thiodiglycolic acid as a possible causative agent of fixed drug eruption provoked only after continuous administration of S-carboxymethyl-L-cysteine: case report and review of reported cases [10].
• The effects of S-carboxymethylcysteine and N-acetylcysteine on the adherence of Moraxella catarrhalis to human pharyngeal epithelial cells [11].
• The inefficacy of penicillamine disulphide and carbocysteine suggests that significant dissociation of the disulphide does not occur in vivo and that the thiol moiety is important in preventing the cystitis [12].
• The results of a double-blind trial on the clinical and functional effects induced by domiodol and S-carboxymethylcysteine (SCMC) on 40 patients with chronic obstructive lung disease are discussed [13].
• Otitis media with effusion and S-carboxymethylcysteine and/or its lysine salt: a critical overview [14].

Biological context of carbocysteine

• It has been claimed that the amino acid derivative carbocisteine is predominantly metabolized by sulfoxidation and that this pathway exhibits a genetic polymorphism [8].
• The technique was applied in a study of the bioavailability of S-(carboxymethyl)-L-cysteine after oral administration to humans [15].
• Conjugation of synthetic peptides to proteins: quantitation from S-carboxymethylcysteine released upon acid hydrolysis [16].
• The validated LC/MS/MS method has been successfully used to a bioequivalence study of two tablet formulations of carbocysteine in healthy volunteers [17].
• After methanol-induced protein precipitation of plasma samples, carbocysteine and the IS were derivatized and subjected to LC/MS/MS analysis using atmospheric pressure chemical ionization [18].

Anatomical context of carbocysteine

• Furthermore, carbocysteine dose dependently repaired the antigen-induced decrease of NEP activity in the tracheal tissue, but it did not influence the bronchial hyperresponsiveness or bronchoalveolar lavage cell component [2].
• In this study, the possible mechanisms of action for the inhibitory effects of S-carboxymethylcysteine on the activation of human neutrophils by N-formyl-methionyl-leucyl-phenylalanine (FMLP) were investigated [19].
• S-carboxymethylcysteine in the fluidification of sputum and treatment of chronic airway obstruction [20].
• Oral N-acetylcysteine or S-carboxymethylcysteine inhibit cigarette smoke-induced hypersecretion of mucus in rat larynx and trachea in situ [21].
• These results suggest that carbocisteine inhibits rhinovirus 2 infection by blocking rhinovirus RNA entry into the endosomes, and inhibits rhinovirus 14 infection by the same mechanism as well as by reducing intercellular adhesion molecule-1 levels [3].

Associations of carbocysteine with other chemical compounds

• In the present study we describe the effects of two mucoregulating drugs, S-carboxymethylcysteine (S-CMC) and ambroxol, on the attachment of NTHI to pharyngeal epithelial cells [22].
• Determination of the sulphoxide metabolites of S-carboxymethyl-L-cysteine by high-performance liquid chromatography with electrochemical detection [23].
• These findings suggest that carbocisteine may normalize the sialyl-Lewis x epitopes expression in mucins through the inhibition of cellular PI-PLC activity in vivo [24].
• Determination of S-carboxymethylcysteine in serum by reversed-phase ion-pair liquid chromatography with column switching following pre-column derivatization with o-phthalaldehyde [15].
• Eight metabolites were separated by HPLC and five identified as degradation products of alkylated glutathione, namely thiodiacetic acid and its sulfoxide, S-carboxymethylcysteine and N-acetyl derivatives of S-carboxymethylcysteine and S-hydroxyethylcysteine.(ABSTRACT TRUNCATED AT 250 WORDS)[25]

Gene context of carbocysteine

• Effects of carbocisteine on altered activities of glycosidase and glycosyltransferase and expression of Muc5ac in SO2-exposed rats [26].
• Preincubation of neutrophils with more than 10 microg/ml of S-carboxymethylcysteine was found to impair neutrophil chemotactic activity toward FMLP, and to inhibit FMLP-mediated neutrophil adherence to pulmonary vascular endothelial cells [19].
• The extent of peptide conjugation was assessed by amino acid analysis after acid hydrolysis, which liberated 1 mol of S-carboxymethylcysteine for each mole of thioether linkage between peptide and protein [27].
• The sulphoxidation of S-carboxymethyl-L-cysteine in COPD [28].
• Reduced airway inflammation and remodeling in parallel with mucin 5AC protein expression decreased by s-carboxymethylcysteine, a mucoregulant, in the airways of rats exposed to sulfur dioxide [29].

Analytical, diagnostic and therapeutic context of carbocysteine

• Disulfide bridge assignments were based on 1) isolation and sequence analysis of S-(carboxymethyl)cysteine-containing peptides and 2) isolation, from unreduced light chains, of peptides containing a disulfide bridge [30].
• A series of mutant KSIs with alternative bases at position 38 have been constructed using a combination of site-directed mutagenesis and chemical modification: Asp-38 to Glu (D38E), His (D38H), and S-(carboxymethyl)cysteine (D38CMC) [31].
• S-(Carboxymethyl)cysteine has been quantified by HPLC on thiol-containing, protected amino acids, peptides, and proteins, after exposure to glyoxal [32].
• Determination of S-carboxymethyl-L-cysteine in plasma by high-performance liquid chromatography with column switching following precolumn derivatization [33].
• The method was utilized to support clinical pharmacokinetic studies of carbocysteine in volunteers following oral administration [18].

References