Derivation, characterisation and analysis of an adverse outcome pathway network for human hepatotoxicity

Toxicology ◽  
2021 ◽  
pp. 152856
Author(s):  
Emma Arnesdotter ◽  
Nicoleta Spinu ◽  
James Firman ◽  
David Ebbrell ◽  
Mark T.D. Cronin ◽  
...  
2020 ◽  
Vol 39 (4) ◽  
pp. 913-922 ◽  
Author(s):  
Gerald T. Ankley ◽  
Brett R. Blackwell ◽  
Jenna E. Cavallin ◽  
Jon A. Doering ◽  
David J. Feifarek ◽  
...  

2019 ◽  
Vol 93 (10) ◽  
pp. 2759-2772 ◽  
Author(s):  
Nicoleta Spinu ◽  
Anna Bal-Price ◽  
Mark T. D. Cronin ◽  
Steven J. Enoch ◽  
Judith C. Madden ◽  
...  

2020 ◽  
Vol 17 (1) ◽  
pp. 147-164 ◽  
Author(s):  
S Jannicke Moe ◽  
Raoul Wolf ◽  
Li Xie ◽  
Wayne G Landis ◽  
Niina Kotamäki ◽  
...  

Chemosphere ◽  
2016 ◽  
Vol 161 ◽  
pp. 372-381 ◽  
Author(s):  
Lihua Yang ◽  
Bingsheng Zhou ◽  
Jinmiao Zha ◽  
Zijian Wang

2021 ◽  
pp. 100206
Author(s):  
Nicoleta Spînu ◽  
Mark T.D. Cronin ◽  
Junpeng Lao ◽  
Anna Bal-Price ◽  
Ivana Campia ◽  
...  

2017 ◽  
Vol 159 (1) ◽  
pp. 159-169 ◽  
Author(s):  
Michelle M. Angrish ◽  
Charlene A. McQueen ◽  
Elaine Cohen-Hubal ◽  
Maribel Bruno ◽  
Yue Ge ◽  
...  

2019 ◽  
Vol 173 (1) ◽  
pp. 32-40 ◽  
Author(s):  
Marylène Rugard ◽  
Xavier Coumoul ◽  
Jean-Charles Carvaillo ◽  
Robert Barouki ◽  
Karine Audouze

Abstract Bisphenol F (BPF) is one of several Bisphenol A (BPA) substituents that is increasingly used in manufacturing industry leading to detectable human exposure. Whereas a large number of studies have been devoted to decipher BPA effects, much less is known about its substituents. To support decision making on BPF’s safety, we have developed a new computational approach to rapidly explore the available data on its toxicological effects, combining text mining and integrative systems biology, and aiming at connecting BPF to adverse outcome pathways (AOPs). We first extracted from different databases BPF-protein associations that were expanded to protein complexes using protein-protein interaction datasets. Over-representation analysis of the protein complexes allowed to identify the most relevant biological pathways putatively targeted by BPF. Then, automatic screening of scientific abstracts from literature using the text mining tool, AOP-helpFinder, combined with data integration from various sources (AOP-wiki, CompTox, etc.) and manual curation allowed us to link BPF to AOP events. Finally, we combined all the information gathered through those analyses and built a comprehensive complex framework linking BPF to an AOP network including, as adverse outcomes, various types of cancers such as breast and thyroid malignancies. These results which integrate different types of data can support regulatory assessment of the BPA substituent, BPF, and trigger new epidemiological and experimental studies.


Nanomaterials ◽  
2021 ◽  
Vol 11 (1) ◽  
pp. 180
Author(s):  
Maud Weiss ◽  
Jiahui Fan ◽  
Mickaël Claudel ◽  
Luc Lebeau ◽  
Françoise Pons ◽  
...  

With the growth of nanotechnologies, concerns raised regarding the potential adverse effects of nanoparticles (NPs), especially on the respiratory tract. Adverse outcome pathways (AOP) have become recently the subject of intensive studies in order to get a better understanding of the mechanisms of NP toxicity, and hence hopefully predict the health risks associated with NP exposure. Herein, we propose a putative AOP for the lung toxicity of NPs using emerging nanomaterials called carbon dots (CDs), and in vivo and in vitro experimental approaches. We first investigated the effect of a single administration of CDs on mouse airways. We showed that CDs induce an acute lung inflammation and identified airway macrophages as target cells of CDs. Then, we studied the cellular responses induced by CDs in an in vitro model of macrophages. We observed that CDs are internalized by these cells (molecular initial event) and induce a series of key events, including loss of lysosomal integrity and mitochondrial disruption (organelle responses), as well as oxidative stress, inflammasome activation, inflammatory cytokine upregulation and macrophage death (cellular responses). All these effects triggering lung inflammation as tissular response may lead to acute lung injury.


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