Oral administration of thioridazine, an inhibitor of perox tsomal p-oxidation, to normal rats from weaning till day 60 causes a small increase of the very long chain fatty acid C26 in brain lipids. Myelination in the brain is decreased. In the genu of the corpus callosum the ratio of non-myelinatedm
Inhibition of peroxisomal beta-oxidation and brain development in rats
β Scribed by Christiane Van Den Branden; Georges Dacremont; Robert Hooghe; Frank Roels
- Publisher
- John Wiley and Sons
- Year
- 1989
- Tongue
- English
- Weight
- 608 KB
- Volume
- 2
- Category
- Article
- ISSN
- 0894-1491
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β¦ Synopsis
Thioridazine, an inhibitor of peroxisomal beta-oxidation, was administered orally to nursing rats during the period of maximal myelination in the pups (8-21 days postnatally). Under the experimental conditions, thioridazine causes accumulation of C24 and C26 fatty acids in pup brain lipids, an effect we consider to be a typical consequence of inhibited peroxisomal beta-oxidation. In the corpus callosum of treated pups, the relationship between axon diameter and myelin sheath thickness is altered compared with matched controls. Thioridazine also induces undernourishment effects in 21 day-old rats. Body and brain weight are severely reduced. Liver peroxisomes show a starvation-type metabolism. Undernourishment is known to influence myelination in developing rat brain. However, known consequences of undernourishment, such as decreased myelin concentration in whole brain, decreased percentage of myelinated fibers, and decreased granule-to-Purkinje cell ratio are not present.
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