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. 2023 Feb;1868(2):159259.
doi: 10.1016/j.bbalip.2022.159259. Epub 2022 Nov 29.

Peroxisomes attenuate cytotoxicity of very long-chain fatty acids

Hanif Ali  1 , Miyu Kobayashi  2 , Katsuya Morito  3 , Rumana Yesmin Hasi  2 , Mutsumi Aihara  2 , Junji Hayashi  2 , Ryushi Kawakami  2 , Koichiro Tsuchiya  3 , Kazunori Sango  4 , Tamotsu Tanaka  5
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Peroxisomes attenuate cytotoxicity of very long-chain fatty acids

Hanif Ali et al. Biochim Biophys Acta Mol Cell Biol Lipids. 2023 Feb.

Abstract

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.

Keywords: Apoptosis; Peroxisome disease; Peroxisome-deficient cells; Very long-chain fatty acids.

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Conflict of interest statement

Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

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