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Protection of erdosteine on smoke‐induced peripheral neutrophil dysfunction both in healthy and in bronchitic smokers
Author(s) -
Ciaccia A.,
Papi A.,
Tschirky B.,
Fregnan B.
Publication year - 1992
Publication title -
fundamental and clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.655
H-Index - 73
eISSN - 1472-8206
pISSN - 0767-3981
DOI - 10.1111/j.1472-8206.1992.tb00133.x
Subject(s) - chemotaxis , chronic bronchitis , in vitro , pharmacology , placebo , chemistry , glutathione , crossover study , medicine , immunology , biochemistry , enzyme , pathology , receptor , alternative medicine
Summary— The purpose of the present study was to determine whether erdosteine and its metabolites (substances containing thiol groups) can prevent the alteration of the chemotactic function of polymorphonuclear cells (PMN) from peripheral blood induced by cigarette smoke of eight healthy non‐smoking volunteers, when incubated in vitro before smoke exposure, and whether oral treatment with erdosteine (900 mg/day) for two weeks might restore the chemotaxis of PMN, either from eight healthy or from 16 chronic bronchitic smokers. The chemotactic stimuli in vitro were casein, lipopolysaccharides (LPS), and formyl‐methionyl‐leucyl‐phenyalanine (FMLP). The results of the study in vitro have confirmed that PMN from non‐smoking volunteers shows a reduced chemotactic responsiveness when exposed in vitro to smoke. This can be partially prevented in a dose‐related manner by pre‐incubation with erdosteine, its metabolites, cysteine, and glutathione (metabolites I and II being at least 10 times more active than the intact substance and the known biological standards also containing thiol groups). The experiment on PMN from healthy smokers (in a double‐blind crossover design versus placebo) has indicated that the chemotaxis can be improved only after treatment with erdosteine. The same observation has been made in the experiment on PMN from smokers affected by chronic bronchitis (in a double‐blind design versus placebo with two distinct groups). In these patients the phagocytic and bactericidal activities of PMN were not affected by the smoke and therefore, neither one was influenced by erdosteine treatment. Since smoke can form free oxidant radicals which have toxic effects on some biological structure, the most likely explanation of the protective action of erdosteine is due to the presence of the blocked SH groups in its molecule which are released during the metabolization process and which exhibits a free radical scavenging action.

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