The medium-chain fatty acid decanoic acid reduces oxidative stress levels in neuroblastoma cells

Janine Mett,Uli Müller

doi:10.1038/s41598-021-85523-9

Abstract

Enhanced oxidative stress is a contributing factor in the pathogenesis of several neurodegenerative disorders such as Alzheimer´s disease. Beneficial effects have been demonstrated for medium-chain fatty acids (MCFAs) nutritionally administered as medium-chain triglycerides (MCTs) or coconut oil (CO). The observed effects on cognitive impairment are generally attributed to the hepatic metabolism of MCFAs, where resulting ketone bodies serve as an alternate energy source to compensate for the impaired glucose utilisation in the human brain. Here we show that the saturated MCFA decanoic acid (10:0) reduces the oxidative stress level in two different neuroblastoma cell lines. Phosphatidylcholine (PC) containing decanoic acid (10:0) (PC10:0/10:0) reduced the cellular H2O2 release in comparison to solvent, L-α-Glycerophosphorylcholine and PC containing the long-chain fatty acid (LCFA) arachidic acid (20:0). This effect seems to be at least partially based on an upregulation of catalase activity, independent of alterations in catalase gene expression. Further, PC10:0/10:0 decreased the intracellular oxidative stress level and attenuated the H2O2-induced cell death. It did not affect the level of the ketone body β-hydroxybutyrate (βHB). These results indicate that decanoic acid (10:0) and possibly MCFAs in general directly reduce oxidative stress levels independent of ketone levels and thus may promote neuronal health.

Highlights

Enhanced oxidative stress is a contributing factor in the pathogenesis of several neurodegenerative disorders such as Alzheimers disease
In order to analyze whether the medium-chain fatty acids (MCFAs) decanoic acid (10:0) influences the oxidative stress level in neuronal cells, we treated neuroblastoma cells with 10 μM of the most abundant phospholipid in mammalian cellular membranes[31], phosphatidylcholine (PC) containing decanoic acid (10:0) in the sn-1 and sn-2 position (1,2-didecanoyl-sn-glycero3-phosphocholine, PC10:0/10:0 compared to both references (PC10):0/10:0)
The total protein content of the homogenates did not vary depending on the different treatments (Supplementary Table S3a). These results indicate the effects of PC10:0/10:0 on H2O2 release and intracellular oxidative stress levels not to be based on an increased metabolism of decanoic acid (10:0) into ketone bodies, but rather on direct cellular effects of this MCFA

Summary

Introduction

Enhanced oxidative stress is a contributing factor in the pathogenesis of several neurodegenerative disorders such as Alzheimers disease. Results The MCFA decanoic acid (10:0) reduces H2O2 release from neuroblastoma cells. The suppressed H 2O2 release and the reduced extracellular H2O2 level of cells treated with PC10:0/10:0 (Fig. 1) might indicate an altered intracellular oxidative stress level.

Results

Conclusion