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Related Concept Videos

Toxicity Testing in Animals01:23

Toxicity Testing in Animals

Toxicity tests in animals are grounded on two main assumptions: first, the effects observed in laboratory animals can be extrapolated to humans, especially when adjusted for body surface area; second, high-dose exposure in animals is essential to identify potential human hazards from lower doses. This is based on the quantal dose-response concept, which faces the challenge of extrapolating results from relatively few test animals to much larger human populations. For example, a 0.01% incidence...

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Related Experiment Video

Updated: Jun 9, 2026

Functional Evaluation of Biological Neurotoxins in Networked Cultures of Stem Cell-derived Central Nervous System Neurons
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Published on: February 5, 2015

In vitro neurotoxicity of methyl iodide.

C J Davenport1, M S Bonnefoi, D A Williams

  • 1Chemical Industry Institute of Toxicology, 6 Davis Drive, PO Box 12137, Research Triangle Park, NC 27709, USA.

Toxicology in Vitro : an International Journal Published in Association with BIBRA
|August 25, 2010
PubMed
Summary

Methyl iodide (MeI) is a neurotoxicant that damages both glial and neuronal cells. Inhibitors like BW755C and NDGA protect against MeI toxicity, suggesting antioxidant mechanisms are involved in its neurotoxicity.

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Area of Science:

  • Neuroscience
  • Toxicology
  • Cell Biology

Background:

  • Methyl iodide (MeI) and related monohalomethanes are known human neurotoxicants.
  • Previous in vivo studies indicate shared toxicity mechanisms among monohalomethanes.

Purpose of the Study:

  • To investigate the in vitro neurotoxicity of methyl iodide (MeI) using neural cell cultures.
  • To explore the protective mechanisms against MeI-induced neurotoxicity.

Main Methods:

  • Primary, dispersed mixed neural cultures from mouse embryos were exposed to MeI.
  • Neurotoxicity was assessed by morphological alterations and lactate dehydrogenase leakage.
  • The effects of inhibitors 3-amino-1-[m-(trifluoromethyl)phenyl]-2-pyrazoline (BW755C) and nordihydroguaiaretic acid (NDGA) were evaluated.

Main Results:

  • MeI caused significant morphological damage and cell death in both glial and neuronal cells.
  • BW755C and NDGA effectively protected neural cultures against MeI toxicity.
  • MeI toxicity was found not to be mediated by glutamate.

Conclusions:

  • Primary neural cultures provide a valid in vitro model for studying monohalomethane neurotoxicity.
  • The protective effects of BW755C and NDGA suggest antioxidant mechanisms may play a role in MeI neurotoxicity.
  • MeI shares toxicity mechanisms with other monohalomethanes, supporting the in vitro model's relevance.