Early-life exposure to methylmercury in wildtype and pdr-1/parkin knockout C. elegans

Ebany J. Martinez-Finley, Sudipta Chakraborty, James C. Slaughter, Michael Aschner

Research output: Contribution to journalArticlepeer-review

24 Scopus citations


We examined the impact of early-life exposure to methylmercury (MeHg) on Caenorhabditis elegans (C. elegans) pdr-1 mutants, addressing gene-environment interactions. We tested the hypothesis that early-life exposure to MeHg and knockout (KO) of pdr-1 (mammalian: parkin/PARK2) exacerbates MeHg toxicity and damage to the dopaminergic (DAergic) system. pdr-1KO worms showed increased lethality and decreased lifespan following MeHg exposure. Mercury (Hg) content, measured with inductively coupled plasma-mass spectrometry was increased in pdr-1KO worms compared to wildtype (N2) controls. 2′7′ dichlorodihydrofluorescein diacetate assay revealed a significant increase in reactive oxygen species in both strains following MeHg exposure; however, while N2 worms showed an increase in skn-1 transcript levels following MeHg exposure, there was no difference in skn-1 induction in pdr-1KO worms. Dopamine-dependent behavioral analysis revealed an effect of MeHg on N2 wildtype worms, but no effect on pdr-1KO worms. Taken together, these results suggest that pdr-1KO worms are more sensitive to MeHg than wildtype worms, but MeHg does not exacerbate behavioral changes related to the absence of pdr-1.

Original languageEnglish (US)
Pages (from-to)1543-1552
Number of pages10
JournalNeurochemical Research
Issue number8
StatePublished - Aug 2013
Externally publishedYes


  • Dopamine
  • Early-life exposure
  • Large amino acid transporter
  • Methylmercury
  • Parkin

ASJC Scopus subject areas

  • Biochemistry
  • Cellular and Molecular Neuroscience


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