Category Research project
  • Toxikologie

Interaction between metabolism and transport of toxicological-relevant substances in the gastrointestinal barrier

Project status
Completed
Project start
Nov 2016
Project end
Sept 2020
Department
Lebensmittelsicherheit

Description and Objective

Polycyclic aromatic hydrocarbons (PAH) comprise a large group of ubiquitously occurring environmental contaminants with the pro-carcinogen benzo[a]pyrene (BP) as best studied representative. The main source of PAH uptake for non-smokers is the daily diet. PAH are only formed in significant amounts during processing (heating and drying) and preparation (e.g. smoking and grilling) of fatty foods such as meat, fish and vegetable oils and fats. In the first period of this project BP its detoxication and hepatobiliary excretion was studied in transporter knockout mice investigating the lack of the two ABC-transporters Breast Cancer Resistance Protein (Bcrp/Abcg2) and Multidrug Resistance-associated Protein 2 (Mrp2/Abcc2). The data showed an important role of these two transporters for BP excretion from the body. Additionally we could show in an in vivo study that a food component, the prominent flavonoid Quercetin, strongly increases the hepatobiliary excretion of BP from the body. However, in reality a mono-exposureExposureTo glossary of humans with BP alone never occurs: always mixtures of PAH are taken up by nutrition. These mixtures consist partly of carcinogenic compounds such as BP, but in percentage terms in substantial proportions of non-carcinogenic PAH such as pyrene and fluoranthene. However, the influence of such mixtures of non-carcinogenic and carcinogenic PAHs on the molecular mechanisms is still inadequately investigated and understood. Accordingly, this project is aimed to investigate the impact of such real PAH mixtures on the metabolism, receptor activity and the genotoxicity of BP based on the results of the last funding period.

Result

Polycyclic aromatic hydrocarbons (PAHs) belong to the group of heat-related contaminants and comprise a large group of organic compounds whose structure consists of at least two fused aromatic rings. PAHs in their original form are lipophilic and low reactive compounds, which are converted to reactive structures only through the process of biotransformation. In non-smokers, the main source of PAH intake is food. The polycyclic compounds found in food result from combustion processes during the processing of, for example, grain products and vegetable oils, and during the smoking of meat products and fish. They are also formed when meat is grilled over open fire. PAHs are always formed in complex mixtures consisting of carcinogenic and non-carcinogenic representatives. However, mixture effects, especially with regard to genotoxic properties of, for example, the already well-studied human carcinogen benzo[a]pyrene (BP), have been little studied so far. To fill these knowledge gaps and to identify combination effects between non-genotoxic and genotoxic PAHs, mixtures of BP with the non-carcinogenic fluoranthene (FA) and pyrene (PYR) in a ratio of 1:2:2.5 were investigated in human HepaRG cells based on the occurrence of PAHs in grilled meat (exposure-based). Analyses included studies of receptor activation of AhR and CAR, gene expression of prominent target genes (CYP1A1 and CYP2B6), and, finally, studies of metabolism of BP and formation of BP-induced DNA damage DNA adducts and DNA double-strand breaks). Our results clearly show that despite significant mixture effects at the molecular level of receptor activation and induction of target gene expression, no substantial mixture effects were observed in the final metabolism and bioactivation of BP. Based on our data, we recommend to investigate and evaluate mixture effects not only by relying on the initiating events but also by examining the biological endpoints such as the influence on metabolism or on the DNA adduct rate.In addition to the exposure-based approach to evaluate the effects of mixtures, effects of 10 structurally-different PAHs (benzo[a]anthracene, benzo[a]pyrene, benzo[b]fluoranthene, benzo[c]phenanthrene, benzo[j]fluoranthene, benzo[k]fluoranthene, dibenzo[a,l]pyrene, fluoranthene, phenanthrene, pyrene) were also investigated first in monoexposure with respect to the interaction with AhR and CAR, the induction of the expression of the target genes CYP1A1/1A2 and CYP2B6, their protein amount and protein activity. Here, small PAHs (up to 4 rings) were found to primarily induce CAR/CYP2B6 and large PAHs (>5 rings) induced AhR/CYP1A1 axis. Following the results, relative potency factors (RPF) for activation of CAR and AhR were calculated for the 10 PAHs based on receptor activation, and then binary mixtures corresponding to BP (RPF=1) were prepared based on the RPFs and receptor activation and target gene expression were reexamined. Finally, the observed effects were compared with the expected effects using three mathematical models. The data from these studies showed that the predictions regarding CAR/CYP2B6 activation were in relatively good agreement, but very little agreement was identified for AhR/CYP1A1 axis activation by the mixtures, which may be associated with the reporter gene assay model or the activation properties of AhR.In summary, the results of our research project show that the analysis of mixture effects is a very complex topic. However, further research in this area is urgently needed, especially research that involves and links multiple endpoints at biological endpoints. Only in this way will it be possible to better evaluate the complex exposure of humans with respect to complex mixtures of xenobiotics.
Type of project

Third-party funded project

Research focus

Nachweis von Kontaminanten und zur Bewertung chemischer Risiken / Wirkungsbezogene Analytik und Risikofrüherkennung

Organisational units and partners

Lead specialist group: Risikobewertungsstrategien (RBS)
Contact persons: Prof. Dr. Dr. Alfonso Lampen, PDshort foroutside lecturer Dr. Stefanie Hessel-Pras
External partner: Biochemisches Institut für Umweltcarcinogene Prof. Dr. Gernot Grimmer Stiftung , University of Eastern Finland, Dr. Margarete Fischer-Bosch-Institut für Klinische Pharmakologie, Signatope GmbH, Karls-Universität

Funding body and grant number

Deutsche Forschungsgemeinschaft e.V.
LA1177/4-4