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Published on: August 25, 2014
Smoking during pregnancy: a risk factor for peripheral neuropathy?
M R Carratù1, A Coluccia, P Borracci
1Department of Pharmacology and Human Physiology, Medical School, University of Bari, Policlinico, Bari, Italy. mrc@farmacol.uniba.it
Prenatal carbon monoxide (CO) exposure in rats leads to reduced myelination in the peripheral nervous system, despite no observed motor skill deficits. This developmental exposure impacts myelin deposition and sphingosine levels.
Area of Science:
- Neuroscience
- Developmental Biology
- Toxicology
Background:
- Developmental exposure to environmental toxins can impact neurological development.
- Carbon monoxide (CO) is a known neurotoxin, but its specific effects on early myelination are not fully understood.
Purpose of the Study:
- To review the outcomes of developmental carbon monoxide (CO) exposure on myelination in rat offspring.
- To investigate the morphological and biochemical changes in the nervous system following prenatal CO exposure.
Main Methods:
- Review of studies on prenatal CO exposure (gestational days 0-20) in rats.
- Analysis of myelin protein patterns using SDS-polyacrylamide gel electrophoresis.
- Analysis of lipid patterns using HPTLC and HPLC methods for sphingomyelin and sphingosine levels.
Main Results:
- Prenatal CO exposure significantly impairs myelin deposition around peripheral axons, causing hypomyelination in juvenile and adult rats.
- Myelin protein and general lipid patterns were unaltered in both peripheral and central nervous systems.
- Increased sphingosine levels were detected in the peripheral nervous system, but not the central nervous system, of CO-exposed rats.
Conclusions:
- Developmental CO exposure causes peripheral hypomyelination and alters sphingolipid metabolism.
- Despite significant morphological and biochemical changes, motor functions remain unaffected in CO-exposed rat offspring.
- These findings highlight a specific vulnerability of peripheral nervous system myelination to prenatal CO insult.
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