Induction of EROD Activity and Genotoxic Effects by Polycyclic Aromatic Hydrocarbons and Resin Acids on the Juvenile Eel (Anguilla anguillaL.)

1997 ◽  
Vol 38 (3) ◽  
pp. 252-259 ◽  
Author(s):  
M. Pacheco ◽  
M.A. Santos
2007 ◽  
Vol 23 (1) ◽  
pp. 55-59 ◽  
Author(s):  
Giovanni Maina ◽  
Marco Manzari ◽  
Antonio Palmas ◽  
Valter Passini ◽  
Francesca Larese Filon

Polycyclic aromatic hydrocarbons have mutagenic and carcinogenic properties and some of them are classified as probable or possible human carcinogens. Aim of this study was to evaluate the genotoxic risk in workers exposed to diesel exaust. Environmental and biological monitoring exposure to polycyclic aromatic hydrocarbons was carried out on fifty-two workers exposed to diesel exhaust. Urinary 1-hydroxypyrene was employed as a biomarker of internal dose. Significant urinary 1-hydroxypyrene differences between smokers and non-smokers were found. Twenty per cent of urinary 1-hydroxypyrene values exceeded benchmark level for genotoxic effect, while the results of environmental monitoring excluded the existence of exposure to polycyclic aromatic hydrocarbons. In the absence of greater knowledge about the relationship between urinary 1-hydroxypyrene and genotoxic effects under the conditions of very low exposure, extreme caution is recommended when this biomarker of internal dose is employed as an indicator of genotoxic risk. Toxicology and Industrial Health 2007; 23: 55—59.


2021 ◽  
Author(s):  
Zelmy Castro-Gálvez ◽  
Montserrat Zaragoza-Ojeda ◽  
Abrahan Hernández-Hernández ◽  
Francisco Arenas-Huertero

Abstract Polycyclic aromatic hydrocarbons (PAH) are organic compounds found in the contaminated atmosphere of Mexico City, where the PAH present with highest concentration is benzo[ghi]perylene [B[ghi]p]. We recently demonstrated that double-stranded breaks in DNA appear after 3h of exposure, whereas cellular changes and activation of aryl hydrocarbon receptor (AHR) pathway occur after 48h in bronchial cells under exposure to B[ghi]p, these findings have led us to explore if the AHR pathway participates in morphological changes and genotoxic effects due to B[ghi]p in human NL-20 bronchial cells. Cells of the NL-20 human bronchial line were exposed to B[ghi]p in the presence, or absence, of the AHR receptor antagonist, CH-223191. Cell viability was quantified by the MTT assay, which revealed 76 and 66% at 6h and 24h, respectively (p<0.001), regardless of the presence of CH-223191. RT-qPCR showed an increase in the expression of the AHR and CYP1A1 cytochrome genes only after 24h of exposure, and the expression was inhibited by CH-223191. Genotoxicity assays revealed the presence of comets, nuclear buds (NB) and DNA fragmentation in cells exposed to B[ghi]p after 6h and in cells exposed to B[ghi]p plus CH-223191 at 24h. These results verify that B[ghi]p induces morphological and genotoxic effects, and these effects are independent of the AHR pathway.


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