PUBLICATION

Low-concentration exposure to glyphosate-based herbicide modulates the complexes of the mitochondrial respiratory chain and induces mitochondrial hyperpolarization in the Danio rerio brain

Authors
Pereira, A.G., Jaramillo, M.L., Remor, A.P., Latini, A., Davico, C.E., da Silva, M.L., Müller, Y.M.R., Ammar, D., Nazari, E.M.
ID
ZDB-PUB-180624-17
Date
2018
Source
Chemosphere   209: 353-362 (Journal)
Registered Authors
Keywords
Behavioral, Cell viability, Central nervous system, Mitochondrial complex activity, Transcript level, Zebrafish
MeSH Terms
  • Animals
  • Electron Transport/physiology*
  • Glycine/analogs & derivatives*
  • Glycine/chemistry
  • Mitochondria/metabolism*
  • Zebrafish
PubMed
29935464 Full text @ Chemosphere
CTD
29935464
Abstract
Glyphosate (N-phosphonomethyl-glycine) (GLY) is the active ingredient of the most used herbicides in the world. GLY is applied in formulated products known as glyphosate-based herbicides (GBH), which could induce effects that are not predicted by toxicity assays with pure GLY. This herbicide is classified as organophosphorus compound, which is known to induce neurotoxic effects. Although this compound is classified as non-neurotoxic by regulatory agencies, acute exposure to GBH causes neurological symptoms in humans. However, there is no consensus in relation to neurotoxic effects of GBH. Thus, the aim of this study was to investigate the neurotoxic effects of the GBH in the zebrafish Danio rerio, focusing on acute toxicity, the activity and transcript levels of mitochondrial respiratory chain complexes, mitochondrial membrane potential, reactive species (RS) formation, and behavioral repertoire. Adult zebrafish were exposed in vivo to three concentrations of GBH Scout®, which contained GLY in formulation (fGLY) (0.065, 1.0 and 10.0 mg L-1 fGLY) for 7 d, and an in vitro assay was performed using also pure GLY. Our results show that GBH induced in zebrafish brain a decrease in cell viability, inhibited mitochondrial complex enzymatic activity, modulated gene expression related to mitochondrial complexes, induced an increase in RS production, promoted hyperpolarization of mitochondrial membrane, and induced behavioral impairments. Together, our data contributes to the knowledge of the neurotoxic effects of GBH. Mitochondrial dysfunction has been recognized as a relevant cellular response that should not be disregarded. Moreover, this study pointed to the mitochondria as an important target of GBH.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping