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Rapid Evaluation of Toxicity of Chemical Compounds Using Zebrafish Embryos
Published on: August 25, 2019
Dithiocarbamates have a common toxic effect on zebrafish body axis formation
Fred Tilton1, Jane K La Du, Meng Vue
1Department of Environmental and Molecular Toxicology, Environmental Health Sciences Center and the Marine and Freshwater Biomedical Sciences Center, Oregon State University, Corvallis, OR 97331, USA.
Toxicology and Applied Pharmacology
|June 27, 2006
Summary
Dithiocarbamate pesticides like sodium metam (NaM) and methylisothiocyanate (MITC) cause zebrafish notochord distortions. Related chemicals and copper chelators also induce these defects, revealing shared molecular pathways in developmental toxicity.
Area of Science:
- Developmental toxicology
- Environmental health
- Zebrafish models
Background:
- Dithiocarbamate (DTC) pesticides, including sodium metam (NaM), and their active ingredient methylisothiocyanate (MITC) are known developmental toxicants.
- Previous studies identified notochord distortions in zebrafish embryos exposed to NaM and MITC.
- The molecular mechanisms underlying the teratogenic effects of these chemical classes require further elucidation.
Purpose of the Study:
- To investigate the teratogenic relationship of isothiocyanates (ITCs), dithiocarbamates (DTCs), and their degradation products at the molecular level in developing zebrafish.
- To explore the role of metal chelation and muscle activity in the observed notochord distortions.
- To identify shared molecular pathways affected by these chemical exposures.
Main Methods:
- Exposure of developing zebrafish embryos to various ITCs, DTCs, and degradation products (e.g., carbon disulfide).
- Assessment of notochord morphology and gene expression patterns (collagen2a1, myoD, no tail) using whole mount in situ hybridization.
- Investigation of the effects of metal chelators (neocuproine) and metals (copper), and muscle relaxants (MS-222) on teratogenic outcomes.
Main Results:
- All tested DTCs induced notochord distortions, while only MITC among ITCs showed this effect. Carbon disulfide also caused distortions.
- Gene expression of collagen2a1 and no tail was perturbed following exposure to DTCs, MITC, and carbon disulfide.
- Copper protected against distortions induced by dimethyl-DTC (DMDTC) and neocuproine (NCu), but not other compounds, suggesting varied mechanisms. Muscle contraction inhibition partially rescued some effects.
Conclusions:
- Distinct but related chemical classes, including DTCs and MITC, share a common toxic effect on zebrafish notochord development.
- While metal chelation is involved in some cases (DMDTC, NCu), it is not the primary mechanism for all tested compounds.
- Perturbation of 'no tail' expression is linked to muscle contractions, whereas collagen2a1 expression reflects earlier developmental impacts.
