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Effects of aflatoxin and fumonisin on gene expression of growth factors and inflammation-related genes in a human hepatocyte cell line

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posted on 2024-09-13, 09:21 authored by Hang Wu, Ya Xu, Yun Yun Gong, John Huntriss, Michael N Routledge

Aflatoxin B1 (AFB1) and fumonisin B1 (FB1) are mycotoxins widely distributed in maize and maized-based products, often occurring together. The implications of co-exposure to aflatoxin and fumonsin for human health are numerous, but a particular concern is the potential of FB1 to modulate AFB1 hepatotoxicity. This study evaluated the toxicity of these mycotoxins, alone or combined, in a human non-tumorigenic liver cell line, HHL-16 cells, and assessed the effects of AFB1 and FB1 on expression of genes involved in immune and growth factor pathways. The results demonstrated that in HHL-16 cells, both AFB1 and FB1 had dose-dependent and time-dependent toxicity, and the combination of them showed a synergistic toxicity in the cells. Moreover, AFB1 caused upregulation of IL6, CCL20, and BMP2, and downregulation of NDP. In combination of AFB1 with FB1, gene expression levels of IL6 and BMP2 were significantly higher compared to individual FB1 treatment, and had a tendency to be higher than individual AFB1 treatment. This study shows that FB1 may increase the hepatoxicity of AFB1 through increasing the inflammatory response and disrupting cell growth pathways.

Funding

This work was supported by the China Scholarship Council; the University of Leeds; and the United Kingdom Environmental Mutagen Society Small Grants Scheme for Feasibility and Pilot Studies 2022.

History

Author affiliation

College of Life Sciences Medicine

Version

  • VoR (Version of Record)

Published in

Mutagenesis

Volume

39

Issue

3

Pagination

181 - 195

Publisher

Oxford University Press (OUP)

issn

0267-8357

eissn

1464-3804

Copyright date

2024

Available date

2024-09-13

Language

en

Deposited by

Dr Michael Routledge

Deposit date

2024-08-23

Data Access Statement

The data will be shared upon request to the corresponding author.

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