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Epigenetic Regulation01:37

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Mitochondrial Epigenetics and Environmental Health: Making a Case for Endocrine Disrupting Chemicals.

Zheng Zhou1, Jaclyn M Goodrich2, Rita S Strakovsky3,4

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Toxicological Sciences : an Official Journal of the Society of Toxicology
|August 11, 2020
PubMed
Summary

Endocrine disrupting chemicals (EDCs) may impact chronic diseases by altering mitochondrial DNA (mtDNA) methylation. Further research is needed to confirm this mechanism and understand EDC-induced epigenetic changes in mitochondria.

Keywords:
endocrine disruptorsenvironmental exposureepigeneticsgene expressionlipidsmethylationmitochondriaoxidative stressredox signalingtranslational

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Area of Science:

  • Environmental Health
  • Molecular Biology
  • Toxicology

Background:

  • Mitochondrial dysfunction is linked to chronic diseases, potentially via mitochondrial DNA (mtDNA) modifications.
  • Epigenetic regulation of mtDNA influences mitochondrial biogenesis and function.
  • Environmental factors like smoking and pollution are associated with altered mtDNA methylation.

Purpose of the Study:

  • To explore mitochondrial DNA epigenetic disruption as a mechanism of action for endocrine disrupting chemicals (EDCs).
  • To review current evidence and limitations regarding EDC impacts on mtDNA methylation.

Main Methods:

  • Review of existing literature on EDCs, mitochondrial function, and epigenetic modifications.
  • Analysis of studies linking environmental factors to mtDNA methylation changes.
  • Examination of EDC effects on nuclear DNA epigenetics and mtDNA methylation modulators.

Main Results:

  • EDCs, including bisphenols and phthalates, directly impact mitochondrial function.
  • EDCs are known modulators of nuclear DNA epigenetics (DNA methylation, histone modifications).
  • EDCs disrupt key modulators of mtDNA methylation, such as DNA methyltransferases and the TFAM/NRF1 pathway.

Conclusions:

  • Mitochondrial DNA epigenetic disruption is a plausible mechanism for EDC toxicity.
  • More research is required to establish a direct link between EDC exposure and mtDNA methylation changes.
  • Understanding these mechanisms is crucial for evaluating EDC risks and developing preventative strategies.