PMID: 2483074Jan 1, 1989Paper

[Mechanism of the mutagenic/carcinogenic action of cigarette smoke at the pulmonary level: enzymatic induction, activation and detoxification].

Annali di igiene : medicina preventiva e di comunità
G Scassellati SforzoliniS Monarca

Abstract

Aryl hydrocarbon hydroxylase (AHH) and dimethylnitrosamine demethylase (DMND) activities in pulmonary and hepatic tissues of male Sprague-Dawley rats were assayed following pretreatment with known inducers (benzo(a)pyrene, 3-methylcholanthrene, Aroclor 1254, phenobarbital) and with mainstream (MS) and side-stream (SS) cigarette smoke condensate and their related fractions. Biochemical assays by spectrophotofluorimetry (AHH activity) and spectrophotometry (DMND activity) and by a biological assay (Ames test) were performed to detect AHH and DMND induction. Ames test proved to be much less sensitive than the spectrophotometric analysis for the AHH determination. Both main-stream and side-stream cigarette smoke condensates and some fractions, containing water-soluble bases, water-insoluble bases, and polycyclic aromatic hydrocarbons, were found to induce AHH activity in lung and liver, the lung being induced to the greatest extent. The highest levels of AHH inducibility were found for the SS-smoke condensate and related fractions. In particular, the insoluble-bases fraction gave the highest induction. On the contrary, pulmonary DMND activity was not affected by pretreatment with the same materials, while hepatic DMND response was ...Continue Reading

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