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Published on: September 27, 2021
Cadmium induces alterations in the human spinal cord morphogenesis
Erica Sarchielli1, Stefania Pacini, Gabriele Morucci
1Department of Anatomy, Histology and Forensic Medicine, University of Firenze, Viale Morgagni 85, 50134, Florence, Italy.
Summary
Cadmium chloride (CdCl2) exposure in human fetal spinal cords significantly reduced motor neurons via apoptosis while increasing glial cells, suggesting a role in neurodegenerative disease development.
Area of Science:
- Neuroscience
- Developmental Biology
- Toxicology
Background:
- The impact of cadmium on the central nervous system and its link to neurodegenerative diseases remain unclear.
- Cadmium chloride (CdCl2) is a toxic heavy metal with potential neurotoxic effects.
Purpose of the Study:
- To investigate the effects of CdCl2 exposure on human fetal spinal cord development.
- To determine if CdCl2 influences motor neuron survival and glial cell proliferation.
Main Methods:
- Human fetal spinal cord explants (10-11 weeks gestational age) were treated with 10 and 100 μM CdCl2 for 24 hours.
- Immunohistochemistry (GFAP, ChAT), Western blot (GFAP, β-Tubulin III, Trk, Caspase 8, PARP), and TUNEL assay were employed.
Main Results:
- CdCl2 caused a dose-dependent decrease in the motor neuron to glial cell ratio in ventral horns.
- Reduced choline acetyltransferase-positive cells (motor neurons) and β-Tubulin III indicate specific motor neuron toxicity.
- Apoptotic pathways were activated in motor neurons (increased Caspase 8, Trk, PARP), while glial fibrillary acidic protein (GFAP) expression increased in glial cells.
Conclusions:
- CdCl2 exposure during human spinal cord development adversely affects neural and glial cell fate.
- These findings suggest a potential role for cadmium in the etiopathogenesis of neurodegenerative diseases.
