Cannabidiol did not induce teratogenicity or neurotoxicity in exposed zebrafish embryos

Chem Biol Interact. 2018 Aug 1;291:81-86. doi: 10.1016/j.cbi.2018.06.008. Epub 2018 Jun 11.


Cannabidiol (CBD) is a non-psychotomimetic compound of the Cannabis sativa that has been used for the treatment of severe epilepsy as well as other diseases of nervous system. However, toxicity studies of CBD have great relevance to guarantee the patients safety. In this context, morphological analyses of zebrafish can contribute to evaluate the teratogenic potential, as well as evaluation of acetylcholinesterase activity and motor activity of zebrafish are valuable tools to verify the neurotoxicity potential. In the present work, we use this methodology to test the toxicity of CBD to zebrafish embryos. No malformation was observed in morphological analysis of embryos exposed to all tested concentrations of CBD. Although, twenty per cent of embryos exposed to maximal dose of CBD (300 μg/L) hatched after 96hpf, while embryos in control solution had already hatched in this period. Embryos exposed to CBD did not show differences in acetylcholinesterase activity, but embryos exposed to CBD 20-300 μg/L were 1.4 up to 1.7-fold more active when compared to the control. Despite that, at 48 hpf, motor activity returned to control values. Our results suggest that the effects observed after CBD exposure are intimately related to CB1 receptor that is present in zebrafish since early stages of development. The present work showed early light effects induced by CBD exposure in concentrations that did not alter biochemical activity.

Keywords: Acetylcholinesterase; Cannabidiol; Motor activity; Neurotoxicity; Teratogenicity; Zebrafish.

MeSH terms

  • Acetylcholinesterase / metabolism
  • Animals
  • Cannabidiol / toxicity*
  • Embryo, Nonmammalian / drug effects*
  • Fertilization
  • Motor Activity / drug effects
  • Neurotoxins / toxicity*
  • Teratogens / toxicity*
  • Zebrafish / embryology*


  • Neurotoxins
  • Teratogens
  • Cannabidiol
  • Acetylcholinesterase