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Biomedical subjects

R Pasquini

Publications and source records attributed to R Pasquini.

101 records · Page 6Linked to original sources
PubMedDate not supplied

[Evaluation of genotoxic and/or co-genotoxic effects in cells exposed in vitro to extremely-low frequency electromagnetic fields].

During the last two decades, concerns have arisen regarding a possible association between extremely-low frequency (ELF) electromagnetic fields (EMF) exposure and cancer incidence (e.g. childhood acute leukaemia, cancer of the nervous system, and lymphomas). In 1979, Wertheimer and Leeper firstly reported an excess of cancer mortality among children living in homes located near power lines and presumably exposed to elevated magnetic fields. Subsequently, a large number of epidemiological studies investigated the possible association between residential or occupational exposure to ELF-EMF and cancer. Several in vivo and in vitro models have been investigated with the effort to determine a link, if any, between such fields and mutagenesis and to determine the possible mechanism of cancer risk. However, a causal relationship between exposure to ELF-EMF and cancer has been suggested but has not been unequivocally demonstrated. In 1998, following an analysis of the results retrieved in the literature, the U.S. National Institute of Environmental Health Sciences proposed to apply a "possible human carcinogen" category (Group 2B) to ELF-EMF. More recently, in 2002, the same classification for ELF-MF was proposed by the International Agency for Research on Cancer. In this in vitro approach, to test the genotoxic and/or co-genotoxic potency of ELF-MF, we used the alkaline single-cell microgel-electrophoresis (comet) assay and the cytokinesis block micronucleus test. Co-exposure assays were performed in the presence of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), 4-nitroquinoline N-oxide (4NQO), benzene, 1,4-benzenediol (1,4-BD), or 1,2,4-benzenetriol (1,2,4-BT). An ELF-MF (50 Hz, 5 mT) was obtained by a system composed of capsulated induction coils. ELF-MF alone was unable to cause direct primary DNA damage. Whereas, an increased extent of DNA damage was observed in cells co-exposed to ELF-MF and MNNG, 1,4-BD, or 1,2,4-BT. An opposite trend was observed in cells treated with 4NQO and co-exposed to ELF-MF. Moreover, the frequency of micronucleated cells in ELF-MF-exposed cells was higher than in control cultures. Our findings suggest that the tested ELF-MF (50 Hz, 5 mT) possess genotoxic (micronucleus test) and co-genotoxic (comet assay) capabilities. The possibility that ELF-MF might interfere with the genotoxic activity of xenobiotics has important implications, since human populations are likely to be exposed to a variety of genotoxic agents concomitantly with exposure to this type of physical agent.

Cells, Cultured↗
PubMedDate not supplied

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

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 only minimally induced by Aroclor and phenobarbital treatment. Twenty-two S12 preparations of surgical lung specimens obtained from smoker and non-smoker cancer patients were also assayed to detect aryl hydrocarbon hydroxylase (AHH), dimethylnitrosamine demethylase (DMND), and glutathione-S-transferase (GST) activities, in both normal and neoplastic lung tissue from the same patients. Pulmonary fractions were also tested for their ability to activate some precarcinogens into mutagenic metabolites in the Ames test. Statistically significant differences were found for AHH and DMND activities between normal and neoplastic tissue of smoker patients. In addition, higher AHH activity in the neoplastic tissue of the smoker group was observed compared with that found in the non-smoker group. No difference were found for GST activity. All the lung S12 preparations were able to metabolize water-soluble bases and water-insoluble bases, derived from main-stream cigarette smoke condensate, into mutagenic agents in the Salmonella test system. However, S12 preparations from smokers group neoplastic tissues were more effective.

Animals↗