Mitochondrial lipids in neurodegeneration

Aufschnaiter, Andreas; Kohler, Verena; Diessl, Jutta; Peselj, Carlotta; Carmona-Gutiérrez, Didac; Keller, Walter; Büttner, Sabrina

doi:10.1007/s00441-016-2463-1

Cited by 72 publications

(59 citation statements)

References 173 publications

(191 reference statements)

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“…Although many studies have sought to understand the dynamic nature of this process, the complete molecular mechanisms underlying it remain unclear (Roy et al, 2015). The lipid composition of the mitochondrial membranes that provides fluidity is probably of major importance in these processes (Aufschnaiter et al, 2017). This is consistent with our findings about the reduction in the length of the fatty acid chains with maternal endurance training as a favourable parameter for the mitochondrial dynamics through a greater mitochondrial membrane fluidity.…”

Section: Discussionsupporting

confidence: 84%

Maternal exercise before and during gestation modifies liver and muscle mitochondria in rat offspring

Farida

Dubouchaud

Hininger

et al. 2019

Journal of Experimental Biology

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It is now well established that the intrauterine environment is of major importance for offspring health during later life. Endurance training during pregnancy is associated with positive metabolic adjustments and beneficial effects on the balance between pro-oxidants and antioxidants (redox state) in the offspring. Our hypothesis was that these changes could rely on mitochondrial adaptations in the offspring due to modifications of the fetal environment induced by maternal endurance training. Therefore, we compared the liver and skeletal muscle mitochondrial function and the redox status of young rats whose mothers underwent moderate endurance training (treadmill running) before and during gestation (T) with those of young rats from untrained mothers (C). Our results show a significant reduction in the spontaneous H 2 O 2 release by liver and muscle mitochondria in the T versus C offspring (P<0.05). These changes were accompanied by alterations in oxygen consumption. Moreover, the percentage of short-chain fatty acids increased significantly in liver mitochondria from T offspring. This may lead to improvements in the fluidity and the flexibility of the membrane. In plasma, glutathione peroxidase activity and protein oxidation were significantly higher in T offspring than in C offspring (P<0.05). Such changes in plasma could represent an adaptive signal transmitted from mothers to their offspring. We thus demonstrated for the first time, to our knowledge, that it is possible to act on bioenergetic function including alterations of mitochondrial function in offspring by modifying maternal physical activity before and during pregnancy. These changes could be crucial for the future health of the offspring.

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Section: Discussionsupporting

confidence: 84%

Maternal exercise before and during gestation modifies liver and muscle mitochondria in rat offspring

Farida

Dubouchaud

Hininger

et al. 2019

Journal of Experimental Biology

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“…For effective interaction between the ER and mitochondria, MAMs have distinctive lipid and protein constituents . Mammalian MAMs have different structure with several enzymes, including PS synthases 1 and 2 (PSS1 and PSS2), acyl CoA:cholesterol acyltransferase/stero‐ O ‐acyltransferase (ACAT1/SOAT1), phosphatidylethanolamine‐ N ‐methyltransferase 2 (PEMT2), diacylglycerol‐ O ‐acyltransferase 2 (DGAT2), and fatty acid CoA ligase 4 (FACL4/ACS4) .…”

Section: Er–mitochondria Crosstalk Functionalitiesmentioning

confidence: 99%

Endoplasmic reticulum–mitochondria crosstalk: from junction to function across neurological disorders

Veeresh

Kaur

Sarmah

et al. 2019

Annals of the New York Academy of Sciences

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The endoplasmic reticulum (ER) and mitochondria are fundamental organelles highly interconnected with a specialized set of proteins in cells. ER–mitochondrial interconnections form specific microdomains, called mitochondria‐associated ER membranes, that have been found to play important roles in calcium signaling and lipid homeostasis, and more recently in mitochondrial dynamics, inflammation, and autophagy. It is not surprising that perturbations in ER–mitochondria connections can result in the progression of disease, especially neurological disorders; hence, their architecture and regulation are crucial in determining the fate of cells and disease. The molecular identity of the specialized proteins regulating ER–mitochondrial crosstalk remains unclear. Our discussion here describes the physical and functional crosstalk between these two dynamic organelles and emphasizes the outcome of altered ER–mitochondrial interconnections in neurological disorders.

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“…c -intact animals; tB -tumorbearing rats in the period of intensive growth of the Guerin's carcinoma; ω-3 -tumor-bearing rats that were administered with ω-3 PUFAs; RA30 -tumorbearing rats that were administered with retinol ace tate in a dose of 30 IU/kg body weight; ra3000tumor-bearing rats that were administered with retinol acetate in a dose of 3000 IU/kg body weight; ω-3+RA30 -tumor-bearing rats that were administered with ω-3 PUFAs and retinol acetate in a dose of 30 IU/kg body weight; ω-3+RA3000 -tumor-bearing rats that were administered with ω-3 PUFas and retinol acetate in a dose of 3000 IU/kg body weight; *statistically significant difference vs. control (Р ≤ 0.05); # statistically significant difference vs. tumor-bearing rats (Р ≤ 0.05) the inner membrane of the liver mitochondria, which leads to swelling of the mitochondria (Fig. 3) and, as a consequence, depolarization of the mitochondrial membranes [1,24]. One of the consequences of this is the hydrolysis of membrane phospholipids by endogenous phospholipase A 2 , whose activity is increased due to an increase in the concentration of Ca 2+ ions.…”

Section: Resultsmentioning

confidence: 99%

Free radical oxidation in liver mitochondria of tumor-bearing rats and its correction by essential lipophilic nutrients

Ketsa¹,

Марченко²

2020

Ukr.Biochem.J

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the role of free radical oxidation in the increase of mitochondrial membranes permeability in organs which are not involved in oncogenesis and the development of the methods for preventing mitochondria dysfunction remain topical problems. In this work, the interconnection of lipid peroxidation (LPO) in liver mitochondrial fraction with the processes of mitochondrial swelling and cytochrome с release to the cytosol under separate and combined administration of ω-3 polyunsaturated fatty acids (PUFAs) and retinol acetate (vitamin a acetate) to rats with transplanted Guerin's carcinoma was studied. During the intensive tumor growth (14 days) the increase of superoxide radical generation and the content of primary (triene conjugates, tc), secondary (ketodienes and coupled trienes, CD+CT) and terminal (Schiff bases) lipid peroxidation products in the mitochondrial fraction of tumor-bearing rats was detected, which contributed to the mitochondrial swelling and cytochrome с release to the cytosol. Separate administration of ω-3 PUFAs to tumor-bearing rats decreased both free radical processes in mitochondrial fraction and mitochondrial swelling. Separate administration of retinol acetate in a high dose (3000 IU/kg of body weight) intensified free radical processes in the mitochondrial fraction of tumor-bearing rats, while administration of retinol acetate in a physiological dose (30 IU/kg of body weight) did not lead to changes compared to tumor-bearing rats that did not receive the drug. The prooxidant effects of retinoid were partially eliminated in the case of combined administration with ω-3 PUFA. K e y w o r d s: liver mitochondrial fraction, lipid peroxidation, cytochrome c, mitochondrial swelling, ω-3 polyunsaturated fatty acids, retinol acetate, Guerin's carcinoma.

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Mitochondrial lipids in neurodegeneration

Cited by 72 publications

References 173 publications

Maternal exercise before and during gestation modifies liver and muscle mitochondria in rat offspring

Maternal exercise before and during gestation modifies liver and muscle mitochondria in rat offspring

Endoplasmic reticulum–mitochondria crosstalk: from junction to function across neurological disorders

Free radical oxidation in liver mitochondria of tumor-bearing rats and its correction by essential lipophilic nutrients

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