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Food Science and Human Wellness 2024, 13(1): 287-298 https://doi.org/10.26599/FSHW.2022.9250024
Research Article | Open Access | Issue | Published: 01 June 2023

Elaidic acid leads to mitochondrial dysfunction via mitochondria-associated membranes triggers disruption of mitochondrial calcium fluxes

Show Author's Information Hui Liu,,  Xuenan Li,  Ziyue Wang,  Lu Li,  Yucai Li,  Haiyang Yan,  Yuan Yuan( )
College of Food Science and Engineering, Jilin University, Changchun 130062, China

Peer review under responsibility of Tsinghua University Press.

Keywords:
Calcium, Endoplasmic reticulum, Elaidic acid (EA), Mitochondria-associated membranes (MAMs), Mitochondria dysfunction
Cite this article:
Liu H, Li X, Wang Z, et al. Elaidic acid leads to mitochondrial dysfunction via mitochondria-associated membranes triggers disruption of mitochondrial calcium fluxes. Food Science and Human Wellness, 2024, 13(1): 287-298. https://doi.org/10.26599/FSHW.2022.9250024
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Abstract Full text About this article

Elaidic acid (EA) stimulation can lead to endoplasmic reticulum stress (ERS), accompanied by a large release of Ca2+, and ultimately the activation of NLRP3 inflammasome in Kupffer cells (KCs). Mitochondrial instability or dysfunction may be the key stimulating factors to activate NLRP3 inflammasome, and sustained Ca2+ transfer can result in mitochondrial dysfunction. We focused on KCs to explore the damage to mitochondria by EA. After EA stimulation, cells produced an oxidative stress (OS) response with a significant increase in ROS release. Immunoprecipitation experiments and the addition of inhibitors revealed that the increase in the level of intracellular Ca2+ led to Ca2+ accumulation in the mitochondrial matrix via mitochondria-associated membranes (MAMs). This was accompanied by a significant release of mROS, loss of MMP and ATP, and a significant increase in mitochondrial permeability transition pore opening, ultimately leading to mitochondrial instability. These findings confirmed the mechanism that EA induced mitochondrial Ca2+ imbalance in KCs via MAM, ultimately leading to mitochondrial dysfunction. Meanwhile, EA induced OS and the decrease of MMP and ATP in rat liver, and significant lesions were found in liver mitochondria. Swelling of the inner mitochondrial cristae and mitochondrial vacuolization occurred, with a marked increase in lipid droplets.


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About this article

Elaidic acid leads to mitochondrial dysfunction via mitochondria-associated membranes triggers disruption of mitochondrial calcium fluxes

Show Author's information Hui Liu,, Xuenan Li, Ziyue Wang, Lu Li, Yucai Li, Haiyang Yan, Yuan Yuan( )
College of Food Science and Engineering, Jilin University, Changchun 130062, China

Peer review under responsibility of Tsinghua University Press.

Abstract

Elaidic acid (EA) stimulation can lead to endoplasmic reticulum stress (ERS), accompanied by a large release of Ca2+, and ultimately the activation of NLRP3 inflammasome in Kupffer cells (KCs). Mitochondrial instability or dysfunction may be the key stimulating factors to activate NLRP3 inflammasome, and sustained Ca2+ transfer can result in mitochondrial dysfunction. We focused on KCs to explore the damage to mitochondria by EA. After EA stimulation, cells produced an oxidative stress (OS) response with a significant increase in ROS release. Immunoprecipitation experiments and the addition of inhibitors revealed that the increase in the level of intracellular Ca2+ led to Ca2+ accumulation in the mitochondrial matrix via mitochondria-associated membranes (MAMs). This was accompanied by a significant release of mROS, loss of MMP and ATP, and a significant increase in mitochondrial permeability transition pore opening, ultimately leading to mitochondrial instability. These findings confirmed the mechanism that EA induced mitochondrial Ca2+ imbalance in KCs via MAM, ultimately leading to mitochondrial dysfunction. Meanwhile, EA induced OS and the decrease of MMP and ATP in rat liver, and significant lesions were found in liver mitochondria. Swelling of the inner mitochondrial cristae and mitochondrial vacuolization occurred, with a marked increase in lipid droplets.

Keywords: Calcium, Endoplasmic reticulum, Elaidic acid (EA), Mitochondria-associated membranes (MAMs), Mitochondria dysfunction

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Received: 24 February 2022
Revised: 18 April 2022
Accepted: 24 June 2022
Published: 01 June 2023
Issue date: January 2024

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© 2024 Beijing Academy of Food Sciences. Publishing services by Tsinghua University Press.

Acknowledgements

This work was supported by fund from the National Natural Science Foundation of China (32172322). The authors gratefully acknowledge the fund support.

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This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

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