Real-world particulate matters induce lung toxicity in rats fed with a high-fat diet: Evidence of histone modifications.

J Hazard Mater

Key Laboratory of Urban Environment and Health, Institute of Urban Environment, Chinese Academy of Sciences, 1799 Jimei Road, Xiamen 361021, China. Electronic address:

Published: August 2021

AI Article Synopsis

  • Exposure to particulate matter (PM) and a high-fat diet (HFD) can worsen lung health, but the mechanisms behind this are not well understood.
  • A study using rats showed that HFD led to significant changes in histone post-translational modifications (PTMs) in the lungs after PM exposure, whereas normal diet rats had minimal changes.
  • Specifically, the study found enhanced PTMs linked to DNA damage in HFD-fed rats, suggesting that combined exposure to PM and HFD causes lung injury by affecting histone modifications and increasing DNA damage.

Article Abstract

Exposure to ambient particulate matters (PMs) has been associated with a variety of lung diseases, and high-fat diet (HFD) was reported to exacerbate PM-induced lung dysfunction. However, the underlying mechanisms for the combined effects of HFD and PM on lung functions remain poorly unraveled. By performing a comparative proteomic analysis, the current study investigated the global changes of histone post-translational modifications (PTMs) in rat lung exposed to long-term, real-world PMs. In result, after PM exposure the abundance of four individual histone PTMs (1 down-regulated and 3 up-regulated) and six combinatorial PTMs (1 down-regulated and 5 up-regulated) were significantly altered in HFD-fed rats while only one individual PTM was changed in rats with normal diet (ND) feeding. Histones H3K18ac, H4K8ac and H4K12ac were reported to be associated with DNA damage response, and we found that these PTMs were enhanced by PM in HFD-fed rats. Together with the elevated DNA damage levels in rat lungs following PM and HFD co-exposure, we demonstrate that PM exposure combined with HFD could induce lung injury through altering more histone modifications accompanied by DNA damage. Overall, these findings will augment our knowledge of the epigenetic mechanisms for pulmonary toxicity caused by ambient PM and HFD exposure.

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Source
http://dx.doi.org/10.1016/j.jhazmat.2021.126182DOI Listing

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