ZFIN ID: ZDB-PUB-191026-4
Polystyrene nanoplastics disrupt glucose metabolism and cortisol levels with a possible link to behavioural changes in larval zebrafish
Brun, N.R., van Hage, P., Hunting, E.R., Haramis, A.G., Vink, S.C., Vijver, M.G., Schaaf, M.J.M., Tudorache, C.
Date: 2019
Source: Communications biology   2: 382 (Journal)
Registered Authors: Schaaf, Marcel J. M.
Keywords: Behavioural ecology, Behavioural methods, Predictive markers, Toxicology, Zebrafish
MeSH Terms:
  • Animals
  • Animals, Genetically Modified
  • Energy Metabolism/drug effects
  • Glucose/metabolism
  • Hydrocortisone/metabolism
  • Larva/drug effects
  • Larva/physiology
  • Motor Activity/drug effects
  • Mutation
  • Nanoparticles/toxicity*
  • Plastics/toxicity
  • Polystyrenes/toxicity*
  • Receptors, Glucocorticoid/genetics
  • Receptors, Glucocorticoid/metabolism
  • Tissue Distribution
  • Water Pollutants, Chemical/toxicity*
  • Zebrafish/genetics
  • Zebrafish/physiology*
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism
PubMed: 31646185 Full text @ Commun Biol
Plastic nanoparticles originating from weathering plastic waste are emerging contaminants in aquatic environments, with unknown modes of action in aquatic organisms. Recent studies suggest that internalised nanoplastics may disrupt processes related to energy metabolism. Such disruption can be crucial for organisms during development and may ultimately lead to changes in behaviour. Here, we investigated the link between polystyrene nanoplastic (PSNP)-induced signalling events and behavioural changes. Larval zebrafish exhibited PSNP accumulation in the pancreas, which coincided with a decreased glucose level. By using hyperglycemic and glucocorticoid receptor (Gr) mutant larvae, we demonstrate that the PSNP-induced disruption in glucose homoeostasis coincided with increased cortisol secretion and hyperactivity in challenge phases. Our work sheds new light on a potential mechanism underlying nanoplastics toxicity in fish, suggesting that the adverse effect of PSNPs are at least in part mediated by Gr activation in response to disrupted glucose homeostasis, ultimately leading to aberrant locomotor activity.