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Updated: Feb 16, 2026

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Measuring Oxidative Stress Resistance of Caenorhabditis elegans in 96-well Microtiter Plates
Published on: May 9, 2015
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[Cellular metabolite controls oxidative stress resistance.]
1Cellular Memory Laboratory, RIKEN, Saitama, Japan.
Summary
D-β-hydroxybutyrate, a ketone body, acts as a class I histone deacetylase (HDAC). This metabolite influences gene transcription and offers protection against oxidative stress by modulating histone modifications.
Area of Science:
- Biochemistry
- Molecular Biology
- Epigenetics
Background:
- Cellular metabolites like acetyl-CoA and NAD+ regulate gene transcription through histone modification.
- D-β-hydroxybutyrate is an endogenous ketone body with known biological functions.
- Histone deacetylases (HDACs) are key epigenetic regulators of gene expression.
Purpose of the Study:
- To review and discuss the molecular basis of ketone body action in transcriptional control.
- To explore the role of D-β-hydroxybutyrate in protecting against oxidative stress.
- To elucidate the epigenetic mechanisms underlying ketone body effects.
Main Methods:
- Literature review of studies on histone modification and epigenetic regulation.
- Analysis of research on D-β-hydroxybutyrate as a metabolite and HDAC.
- Discussion of molecular pathways linking ketone bodies to gene transcription and oxidative stress response.
Main Results:
- D-β-hydroxybutyrate functions as a class I histone deacetylase (HDAC).
- Ketone bodies can modulate gene transcription by altering histone acetylation patterns.
- Evidence suggests a role for D-β-hydroxybutyrate in cellular protection against oxidative damage.
Conclusions:
- D-β-hydroxybutyrate represents a key link between cellular metabolism and epigenetic regulation.
- Understanding the role of ketone bodies in transcriptional control offers insights into metabolic diseases and aging.
- Further research into D-β-hydroxybutyrate's HDAC activity may reveal therapeutic strategies for oxidative stress-related conditions.
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