Table 1 Potential developmental neurotoxicity chemicals to be tested in aggregating brain cell cultures
From: Toward a 3D model of human brain development for studying gene/environment interactions
Chemical | Exposure | Toxic effects and/or main mechanisms of toxicity |
|---|---|---|
Aspartame | Food additive | Excitotoxicity mainly through activation of the NMDA-R, reduction of acetylcholine esterase activity and increase in reactive oxygen species |
Bisphenol A | Plastic additive | Endocrine disrupter at very low doses, can suppress cell proliferation, can induce apoptotic cell death and produce reactive oxygen species |
Cadmium chloride | Environmental contaminant, smoking | Causes oxidative stress and affects genes involved in cell cycle regulation |
Carbaryl | Pesticide | Affects neurite outgrowth, inhibits nitric oxide synthesis and inhibits acetylcholine esterase |
Chlorpyrifos | Pesticide | Inhibits acetylcholine esterase, induces damage to RNA and DNA synthesis, oxidative stress, astroglial proliferation and cell differentiation |
Lamotrigine | Anti-convulsant drug | Interferes with the voltage gated sodium channels and has shown teratogenic effects in some studies |
Lead chloride | Environmental contaminant | Associated with numerous adverse effects in the central nervous system, including destruction of the blood-brain barrier, loss of neurons, gliosis and oxidative stress |
Lindane | Pesticide | Inhibits acetylcholine esterase, noradrenalin uptake, GABA neurotransmission and blocks glycine receptors |
Maneb | Pesticide | Inhibits GABA synthesis, causes loss of dopaminergic and GABAergic neurons, decreases ATP levels and causes oxidative stress |
Trichloroethylene | Environmental contaminant | Associated with adverse effects in the central nervous system, induces loss of dopaminergic neurons and oxidative stress |
Valproic acid | Antiepileptic drug | Recognized as a teratogenic compound, modifies the release of GABA |