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ID 117825
Author
Ali, Hanif Tokushima University
Kobayashi, Miyu Tokushima University
Morito, Katsuya Tokushima University
Hasi, Rumana Yesmin Tokushima University
Sango, Kazunori Tokyo Metropolitan Institute of Medical Science
Keywords
Peroxisome disease
Very long-chain fatty acids
Peroxisome-deficient cells
Apoptosis
Content Type
Journal Article
Description
One of the major functions of peroxisomes in mammals is oxidation of very long-chain fatty acids (VLCFAs). Genetic defects in peroxisomal β-oxidation result in the accumulation of VLCFAs and lead to a variety of health problems, such as demyelination of nervous tissues. However, the mechanisms by which VLCFAs cause tissue degeneration have not been fully elucidated. Recently, we found that the addition of small amounts of isopropanol can enhance the solubility of saturated VLCFAs in an aqueous medium. In this study, we characterized the biological effect of extracellular VLCFAs in peroxisome-deficient Chinese hamster ovary (CHO) cells, neural crest-derived pheochromocytoma cells (PC12), and immortalized adult Fischer rat Schwann cells (IFRS1) using this solubilizing technique. C20:0 FA was the most toxic of the C16–C26 FAs tested in all cells. The basis of the toxicity of C20:0 FA was apoptosis and was observed at 5 μM and 30 μM in peroxisome-deficient and wild-type CHO cells, respectively. The sensitivity of wild-type CHO cells to cytotoxic C20:0 FA was enhanced in the presence of a peroxisomal β-oxidation inhibitor. Further, a positive correlation was evident between cell toxicity and the extent of intracellular accumulation of toxic FA. These results suggest that peroxisomes are pivotal in the detoxification of apoptotic VLCFAs by preventing their accumulation.
Journal Title
Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids
ISSN
13881981
NCID
AA11522965
AA11300409
Publisher
Elsevier
Volume
1868
Issue
2
Start Page
159259
Published Date
2022-11-29
Rights
© 2022. This manuscript version is made available under the CC-BY-NC-ND 4.0 license https://creativecommons.org/licenses/by-nc-nd/4.0/
EDB ID
DOI (Published Version)
URL ( Publisher's Version )
FullText File
language
eng
TextVersion
Author
departments
Bioscience and Bioindustry
Pharmaceutical Sciences