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Trichostatin A Shows Transient Protection from Chronic Alcohol-Induced Reactive Oxygen Species (ROS) Production in

Tiyash Parira1, Gloria Figueroa1, Sherly Granado1

  • 1Department of Immunology and Nano-Medicine, Herbert Wertheim College of Medicine, Florida International University, Miami, FL, 33199, USA.

Journal of Alcoholism and Drug Dependence
|January 1, 2019
PubMed
Abstract

Insights

Trichostatin A (TSA) offers transient protection against alcohol-induced ROS in human dendritic cells, but long-term exposure causes toxicity. The antioxidant regulator Nrf2 may mediate TSA's effects, warranting further investigation.

Area of Science:

  • Immunology
  • Cell Biology
  • Toxicology

Background:

  • Chronic alcohol exposure induces oxidative stress (ROS) in immune cells.
  • Dendritic cells play a crucial role in immune responses.
  • Histone deacetylase (HDAC) inhibitors are being explored for therapeutic potential.

Purpose of the Study:

  • To investigate if Trichostatin A (TSA) can inhibit or reverse alcohol-induced ROS in human monocyte-derived dendritic cells (MDDCs).
  • To examine the impact of alcohol and TSA on ROS production and the antioxidant regulator Nrf2 in MDDCs.

Main Methods:

  • MDDCs were chronically treated with varying concentrations of alcohol (0.1% and 0.2%).
  • Intracellular, extracellular, and total ROS levels were measured using DCF-DA and imaging flow cytometry.
  • Nrf2 expression was analyzed via qRT-PCR and western blot; in silico analysis of relevant genes was performed.

Main Results:

  • Alcohol rapidly increased intracellular ROS levels in MDDCs.
  • TSA demonstrated a transient protective effect, reducing ROS only up to 15 minutes post-treatment.
  • Chronic alcohol exposure upregulated Nrf2 expression in a dose-dependent manner, an effect enhanced by TSA at higher alcohol concentrations.

Conclusions:

  • TSA provides a temporary protective effect against alcohol-induced ROS in MDDCs.
  • Prolonged co-exposure to alcohol and TSA leads to cellular toxicity.
  • Nrf2 may be involved in TSA's mechanism, but further research is needed to elucidate the molecular pathways.
Keywords:
Human dendritic cellsImaging flow cytometryOxidative stressReactive oxygen speciesTrichostatin A

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