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The liver is an important organ in vertebrates that plays an essential role in metabolism. It is also responsible for storing and redistributing nutrients such as carbohydrates, fats, and vitamins in the body. Additionally, the liver releases bile salts which are critical for digesting food and eliminating toxic metabolites from the body.
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An inflammatory response is a localized, nonspecific immune reaction that occurs when a tissue is injured. It is characterized by redness, swelling, heat, and pain, which are commonly called the cardinal signs and symptoms of inflammation. Inflammation can sometimes result in a loss of function.
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Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl...
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Multicellular organisms contain a variety of structurally and functionally distinct cell types, but the DNA in all the cells originated from the same parent cells. The differences in the cells can be attributed to the differential gene expression. Liver cells, whose functions include detoxification of blood, production of bile to metabolize fats, and synthesis of proteins essential for metabolism, must express a specific set of genes to perform their functions. Gene expression also varies with...
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Related Experiment Video

Updated: Jun 3, 2025

Development of an Ethanol-induced Fibrotic Liver Model in Zebrafish to Study Progenitor Cell-mediated Hepatocyte Regeneration
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Ethyltoluenes Regulate Inflammatory and Cell Fibrosis Signaling in the Liver Cell Model.

Suryakant Niture1,2, Sashi Gadi1, Hieu Hoang1

  • 1The Julius L. Chambers Biomedical/Biotechnology Research Institute (JLC-BBRI), North Carolina Central University (NCCU), Durham, NC 27707, USA.

Toxics
|January 8, 2025
PubMed
Summary

Ethyltoluenes (ETs) from crude oil exposure impact liver cells, increasing oxidative stress and inflammation. While not causing steatosis, ETs alter cell metabolism and fibrosis markers, potentially disrupting liver function.

Keywords:
cell proliferationethyltoluenesfibrosisinflammationliver cell modelssteatosis

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Area of Science:

  • Toxicology
  • Hepatology
  • Environmental Health

Background:

  • Crude oil naphtha fraction C9 alkylbenzenes, particularly ethyltoluenes (ETs), are environmental contaminants.
  • Occupational and environmental exposure to ETs can occur via inhalation and ingestion.
  • Previous studies indicate ETs target the respiratory tract and liver, causing lesions.

Purpose of the Study:

  • Investigate the impact of low concentrations of ET isomers (2-ET, 3-ET, 4-ET) on liver cell models.
  • Assess effects on cell metabolism, inflammation, steatosis, and fibrosis signaling.
  • Utilize HepaRG, HepG2, and SK-Hep1 cell lines for in vitro analysis.

Main Methods:

  • Dose-dependent exposure of liver cell models to individual ET isomers.
  • Real-time monitoring of cell survival and proliferation.
  • Measurement of reactive oxygen species (ROS) production.
  • Analysis of inflammatory, metabolic, lipogenesis, and fibrosis gene expression.
  • Assessment of mitochondrial respiration and cellular energetics.

Main Results:

  • ET exposure increased ROS production and modulated inflammatory gene expression (CAT, SOD1, CXCL8, IL1B, HMOX1, NAT1, STAT3).
  • Cellular energetics and metabolic gene expression (CYP1A1, CYP1A2, CYP2D6, CYP2E1, CYP3A4, CYP3B4, VEGFA) were upregulated.
  • No significant changes in lipogenesis-related gene expression or cell steatosis were observed.
  • ET exposure modulated fibrosis markers (AST, FGF-23, Cyt-7 p21, TGFβ, TIMP2, MMP2), particularly with chronic 2-ET exposure.

Conclusions:

  • Ethyltoluenes impact liver cell metabolism, inflammation, and fibrosis signaling.
  • ETs increase oxidative stress and alter mitochondrial respiration in liver cells.
  • While ETs do not induce steatosis, they may dysregulate liver function by targeting fibrosis pathways.