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Metabolomic changes induced by nicotine in adult zebrafish skeletal muscle

Cristian Gómez-Canela1, Eva Prats2, Silvia Lacorte1

  • 1Department of Environmental Chemistry, IDAEA-CSIC, Jordi Girona 18-26, 08034 Barcelona, Catalonia, Spain.

Ecotoxicology and Environmental Safety
|August 25, 2018
PubMed

Insights

Nicotine exposure did not cause muscle damage in adult zebrafish, despite causing changes in metabolites similar to human exercise responses. This suggests adult zebrafish muscle-type nicotinic acetylcholine receptors (nAChRs) may be less permeable to calcium, preventing toxicity.

Area of Science:

  • Toxicology
  • Neuroscience
  • Zebrafish models

Background:

  • Acute exposure to nicotinic agonists can cause myotoxicity in zebrafish embryos.
  • Nicotine acetylcholine receptors (nAChRs) are implicated in muscle function.
  • Adult zebrafish muscle-type nAChRs may differ in calcium permeability compared to embryonic forms.

Purpose of the Study:

  • To evaluate the potential myotoxicity of nicotine, a model nAChR agonist, on adult zebrafish muscle tissue.
  • To investigate the effects of varying nicotine concentrations and exposure durations on adult zebrafish muscle.
  • To analyze metabolic changes in adult zebrafish following nicotine exposure.

Main Methods:

  • Adult zebrafish were exposed to nicotine at different concentrations and time points (2, 6, 24 hours).
  • Liquid chromatography coupled to high-resolution mass spectrometry (LC-HRMS) was used for metabolite profiling.
  • Chemometric tools, including ROI-MCR-ALS and ASCA, were applied to analyze LC-HRMS data.

Main Results:

  • Nicotine exposure induced significant, concentration- and time-dependent changes in metabolite profiles.
  • Metabolic changes observed were similar to those seen in humans after strenuous exercise, linked to hyperlocomotion.
  • No myotoxicity was detected in adult zebrafish muscle tissue, even at high nicotine concentrations or prolonged exposure.

Conclusions:

  • Adult zebrafish muscle tissue is not susceptible to nicotine-induced myotoxicity.
  • Observed metabolic alterations are likely secondary to nicotine-induced hyperlocomotion, not direct muscle damage.
  • The lack of myotoxicity may be attributed to the reduced calcium permeability of adult muscle-type nAChRs.
Keywords:
ASCALC-HRMSNicotineROI-MCRZebrafish

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