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Effects of methyl and inorganic mercury exposure on genome homeostasis and mitochondrial function in Caenorhabditis elegans.

Publication ,  Journal Article
Wyatt, LH; Luz, AL; Cao, X; Maurer, LL; Blawas, AM; Aballay, A; Pan, WKY; Meyer, JN
Published in: DNA repair
April 2017

Mercury toxicity mechanisms have the potential to induce DNA damage and disrupt cellular processes, like mitochondrial function. Proper mitochondrial function is important for cellular bioenergetics and immune signaling and function. Reported impacts of mercury on the nuclear genome (nDNA) are conflicting and inconclusive, and mitochondrial DNA (mtDNA) impacts are relatively unknown. In this study, we assessed genotoxic (mtDNA and nDNA), metabolic, and innate immune impacts of inorganic and organic mercury exposure in Caenorhabditis elegans. Genotoxic outcomes measured included DNA damage, DNA damage repair (nucleotide excision repair, NER; base excision repair, BER), and genomic copy number following MeHg and HgCl2 exposure alone and in combination with known DNA damage-inducing agents ultraviolet C radiation (UVC) and hydrogen peroxide (H2O2), which cause bulky DNA lesions and oxidative DNA damage, respectively. Following exposure to both MeHg and HgCl2, low-level DNA damage (∼0.25 lesions/10kb mtDNA and nDNA) was observed. Unexpectedly, a higher MeHg concentration reduced damage in both genomes compared to controls. However, this observation was likely the result of developmental delay. In co-exposure treatments, both mercury compounds increased initial DNA damage (mtDNA and nDNA) in combination with H2O2 exposure, but had no impact in combination with UVC exposure. Mercury exposure both increased and decreased DNA damage removal via BER. DNA repair after H2O2 exposure in mercury-exposed nematodes resulted in damage levels lower than measured in controls. Impacts to NER were not detected. mtDNA copy number was significantly decreased in the MeHg-UVC and MeHg-H2O2 co-exposure treatments. Mercury exposure had metabolic impacts (steady-state ATP levels) that differed between the compounds; HgCl2 exposure decreased these levels, while MeHg slightly increased levels or had no impact. Both mercury species reduced mRNA levels for immune signaling-related genes, but had mild or no effects on survival on pathogenic bacteria. Overall, mercury exposure disrupted mitochondrial endpoints in a mercury-compound dependent fashion.

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Published In

DNA repair

DOI

EISSN

1568-7856

ISSN

1568-7864

Publication Date

April 2017

Volume

52

Start / End Page

31 / 48

Related Subject Headings

  • Ultraviolet Rays
  • Mitochondria
  • Methylmercury Compounds
  • Mercury
  • Kinetics
  • Hydrogen Peroxide
  • Homeostasis
  • Developmental Biology
  • DNA, Helminth
  • DNA Repair
 

Citation

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Chicago
ICMJE
MLA
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Wyatt, L. H., Luz, A. L., Cao, X., Maurer, L. L., Blawas, A. M., Aballay, A., … Meyer, J. N. (2017). Effects of methyl and inorganic mercury exposure on genome homeostasis and mitochondrial function in Caenorhabditis elegans. DNA Repair, 52, 31–48. https://doi.org/10.1016/j.dnarep.2017.02.005
Wyatt, Lauren H., Anthony L. Luz, Xiou Cao, Laura L. Maurer, Ashley M. Blawas, Alejandro Aballay, William K. Y. Pan, and Joel N. Meyer. “Effects of methyl and inorganic mercury exposure on genome homeostasis and mitochondrial function in Caenorhabditis elegans.DNA Repair 52 (April 2017): 31–48. https://doi.org/10.1016/j.dnarep.2017.02.005.
Wyatt LH, Luz AL, Cao X, Maurer LL, Blawas AM, Aballay A, et al. Effects of methyl and inorganic mercury exposure on genome homeostasis and mitochondrial function in Caenorhabditis elegans. DNA repair. 2017 Apr;52:31–48.
Wyatt, Lauren H., et al. “Effects of methyl and inorganic mercury exposure on genome homeostasis and mitochondrial function in Caenorhabditis elegans.DNA Repair, vol. 52, Apr. 2017, pp. 31–48. Epmc, doi:10.1016/j.dnarep.2017.02.005.
Wyatt LH, Luz AL, Cao X, Maurer LL, Blawas AM, Aballay A, Pan WKY, Meyer JN. Effects of methyl and inorganic mercury exposure on genome homeostasis and mitochondrial function in Caenorhabditis elegans. DNA repair. 2017 Apr;52:31–48.
Journal cover image

Published In

DNA repair

DOI

EISSN

1568-7856

ISSN

1568-7864

Publication Date

April 2017

Volume

52

Start / End Page

31 / 48

Related Subject Headings

  • Ultraviolet Rays
  • Mitochondria
  • Methylmercury Compounds
  • Mercury
  • Kinetics
  • Hydrogen Peroxide
  • Homeostasis
  • Developmental Biology
  • DNA, Helminth
  • DNA Repair