Comparative study of diesel and biodiesel exhausts on lung oxidative stress and genotoxicity in rats
Creators
- 1. Univ. Grenoble Alpes, CEA, CNRS, INAC, SyMMES/CIBEST, F-38000 Grenoble (France)
- 2. Normandie Univ, UNICAEN, UNIROUEN, ABTE, 14000 Caen et 76000, Rouen (France)
- 3. CERTAM, 1 Rue Joseph Fourier, 76800 Saint-Etienne du Rouvray (France)
- 4. Unité de Chimie Environnementale et Interactions sur le Vivant, EA4492, Université du Littoral Côte d'Opale, Dunkerque (France)
- 5. Institut de Recherches en Santé, Environnement et Travail (IRSET), UMR INSERM U1085, Faculté de Pharmacie, 35043 Rennes (France)
Description
Highlights: • Rats were repeatedly exposed to diesel exhaust up- or downstream of a particle filter. • Exposure to diesel or biodiesel induces only low levels of DNA damage. • Parameters related to telomeres maintenance and to oxidative stress are not altered. • Diesel down-regulates the expression of some genes involved in genotoxicity. • Significant effects downstream of the filter suggest a toxicity of the gaseous phase. The contribution of diesel exhaust to atmospheric pollution is a major concern for public health, especially in terms of occurrence of lung cancers. The present study aimed at addressing the toxic effects of a repeated exposure to these emissions in an animal study performed under strictly controlled conditions. Rats were repeatedly exposed to the exhaust of diesel engine. Parameters such as the presence of a particle filter or the use of gasoil containing rapeseed methyl ester were investigated. Various biological parameters were monitored in the lungs to assess the toxic and genotoxic effects of the exposure. First, a transcriptomic analysis showed that some pathways related to DNA repair and cell cycle were affected to a limited extent by diesel but even less by biodiesel. In agreement with occurrence of a limited genotoxic stress in the lungs of diesel-exposed animals, small induction of γ-H2AX and acrolein adducts was observed but not of bulky adducts and 8-oxodGuo. Unexpected results were obtained in the study of the effect of the particle filter. Indeed, exhausts collected downstream of the particle filter led to a slightly higher induction of a series of genes than those collected upstream. This result was in agreement with the formation of acrolein adducts and γH2AX. On the contrary, induction of oxidative stress remained very limited since only SOD was found to be induced and only when rats were exposed to biodiesel exhaust collected upstream of the particle filter. Parameters related to telomeres were identical in all groups. In summary, our results point to a limited accumulation of damage in lungs following repeated exposure to diesel exhausts when modern engines and relevant fuels are used. Yet, a few significant effects are still observed, mostly after the particle filter, suggesting a remaining toxicity associated with the gaseous or nano-particular phases.
Availability note (English)
Available from http://dx.doi.org/10.1016/j.envpol.2017.12.077Additional details
Identifiers
- DOI
- 10.1016/j.envpol.2017.12.077;
- PII
- S0269749117330014;
Publishing Information
- Journal Title
- Environmental Pollution (1987)
- Journal Volume
- 235
- Journal Page Range
- p. 514-524
- ISSN
- 0269-7491
- CODEN
- ENPOEK
INIS
- Country of Publication
- United Kingdom
- Country of Input or Organization
- International Atomic Energy Agency (IAEA)
- INIS RN
- 54075515
- Subject category
- S54: ENVIRONMENTAL SCIENCES;
- Descriptors DEI
- AIR POLLUTION; BIODIESEL FUELS; BRASSICA; CELL CYCLE; DIESEL ENGINES; DNA DAMAGES; DNA REPAIR; ESTERS; FILTERS; GENES; LUNGS; MAINTENANCE; NEOPLASMS; OXIDATION; PUBLIC HEALTH; RATS; TELOMERES; TOXICITY
- Descriptors DEC
- ALTERNATIVE FUELS; ANIMALS; BIOFUELS; BIOLOGICAL RECOVERY; BIOLOGICAL REPAIR; BODY; CHEMICAL REACTIONS; DISEASES; ENGINES; FOOD; FUELS; HEAT ENGINES; INTERNAL COMBUSTION ENGINES; LIQUID FUELS; MAGNOLIOPHYTA; MAGNOLIOPSIDA; MAMMALS; ORGANIC COMPOUNDS; ORGANS; PLANTS; POLLUTION; REPAIR; RESPIRATORY SYSTEM; RODENTS; VEGETABLES; VERTEBRATES
Optional Information
- Copyright
- Copyright (c) 2018 Elsevier Ltd. All rights reserved.