Uptake of ethanolamine in neuronal and glial cell cultures

Massarelli, A; Dainous, Francine; Hoffmann, Dieter; Mykita, S.; Freysz, L.; Dreyfus, H.; Massarelli, R.

doi:10.1007/bf00965162

Cited by 11 publications

(3 citation statements)

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“…The temporal cortex shows the most severe reduction in Etn [ 11,281, with the largest degree of neuronal loss and the highest incidence of the neuropathologic markers of A. D. [24]. Thus, the depletion of Etn could be due to the severe loss of neurons, which are known to have a higher affinity for Etn uptake than glial cells [26]. Other mechanisms contributing to the Etn reduction found in A. D., but not yet examined, could include decreased blood levels of Etn, or its decreased absorption from the intestinal lumen.…”

Section: Discussionmentioning

confidence: 99%

Effects of ethanolamine (ETN) Administration on etn and choline (CH) levels in plasma, brain extracellular fluid (ECF) and brain tissue, and on brain phospholipid levels in rats: An in vivo study

Marshall

Micheli

Богданов

et al. 1996

Neurosci. Res. Comm.

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The sources and fates of brain ethanolamine (Etn) are poorly known and the effects of its administration have not been investigated, even though cortical levels are known to be reduced in certain neurodegenerative diseases. We studied the effect of different Etn doses (10−3, 5 × 10−3 and 10−2 mol/kg, i. p.) on its and choline's (Ch) levels in arterial plasma and brain extracellular fluid (ECF) of awake rats. We also studied its effects on brain levels of Etn, Ch, and their respective major phospholipids. Etn administration caused dose dependent increases in Etn levels within both plasma and brain ECF. For the 10−2 mol/kg dose, Etn levels were significantly (p<0.01) greater than pre‐injection values in both the plasma and ECF. Whole brain Etn and phosphatidylethanolamine were also significantly (p<0.05) increased by 10−2 mol/kg Etn. Exogenous Etn significantly (p<0.05) increased Ch levels in plasma and whole brain; Etn also increased brain ECF Ch levels. Our data show for the first time that circulating Etn can act as a source of brain Ch. Metabolic pathways that might mediate the increases in Etn and Ch are discussed, as are possible mechanisms of the decreases in brain Etn seen in Alzheimer's disease.

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Section: Discussionmentioning

confidence: 99%

Effects of ethanolamine (ETN) Administration on etn and choline (CH) levels in plasma, brain extracellular fluid (ECF) and brain tissue, and on brain phospholipid levels in rats: An in vivo study

Marshall

Micheli

Богданов

et al. 1996

Neurosci. Res. Comm.

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“…The concentration of myo -inositol selected was based on the findings from Novak et al, who demonstrated that differentiated human central nervous system neurons (NT2-N neurons) have a maximal velocity of inositol uptake ( V max ) of 3.7 nmol/mg-protein/h when treated with various concentrations of inositol ranging from 0 to 500 μM. The concentration of ethanolamine was chosen on the basis of a report showing that the maximum ethanolamine uptake for neuronal cells is 41.4 pmol/mg-protein/min . A combination of myo -inositol + ethanolamine treatment (ME) was investigated since PE-Pls biosynthesis requires the ethanolamine-derived CDP-ethanolamine in the pathway, and our laboratory has previously shown that this combination treatment leads to enhanced biosynthesis of ethanolamine phospholipids in rat brain in vivo . − The 24 h optimal incubation time was determined in a separate series of experiments in which cells were cultured in growth medium supplemented with ME for 24, 48, and 72 h. The amounts of PE-Pls (nmol/mg protein) obtained with these incubation times were not significantly different ( p < 0.05; data not shown).…”

Section: Methodsmentioning

confidence: 99%

Influence of Myo-inositol Plus Ethanolamine on Plasmalogens and Cell Viability during Oxidative Stress

Sibomana

Grobe

DelRaso

et al. 2019

Chem. Res. Toxicol.

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Previously, we demonstrated that treatment of rats with myo-inositol plus ethanolamine (ME) elevated brain ethanolamine plasmalogens (PE-Pls) and protected against phosphineinduced oxidative stress. Here we tested the hypothesis that ME treatment elevates PE-Pls in a neuro-2A (N2A) cell culture system and protects against hydrogen peroxide (H 2 O 2 )-induced oxidative stress, and we assessed the effects of treatments using myo-inositol with or without (+/−) ethanolamine on ethanolamine phospholipids (PLs) and cell viability following H 2 O 2 exposure. Cells were treated with equimolar amounts (500 μM) of myo-inositol, ethanolamine (Etn), or their combination (ME) for 24 h, followed by an additional 24 h exposure to 650 μM H 2 O 2 . NMR analyses evaluated the treatment effects on Etn PLs, while LC-MS/MS analyses assessed the molecular species of Etn PLs preferentially affected by ME and H 2 O 2 treatments, especially PE-Pls and their degradation byproductslysophosphatidylethanolamine (LPE) and glycerophosphoethanolamine (GPE). Only ME influenced the cellular levels of PLs. ME yielded a 3-fold increase in PE-Pls and phosphatidylethanolamine (PE) (p < 0.001) and a preferential 60% increase in PE-Pls containing saturated and monounsaturated fatty acids (SFA+MUFA), while polyunsaturated fatty acid (PUFA) species increased by only 10%. Exposing cells to 650 μM H 2 O 2 caused a significant cell death (56% viability), a 27% decrease in PE-Pls, a 201% increase in PUFA-rich LPE, and a ca. 3-fold increase in GPE. H 2 O 2 had no impact on PE, suggesting that LPE and GPE were primarily the byproducts of PE-Pls (not PE) degradation. Surprisingly, ME pretreatment ameliorated H 2 O 2 effects and significantly increased cell survival to 80% (p < 0.05). Cellular PE-Pls levels prior to H 2 O 2 treatment were highly correlated (R 2 = 0.95) with cell survival, suggesting a relationship between PE-Pls and cell protection. Data suggest that a preferential increase in PE-Pls containing SFA+MUFA species may protect cells from oxidative stress. Such studies aid in our understanding of the neuroprotective mechanisms that may be associated with plasmalogens and the relevance of these phospholipids to neurodegenerative diseases/disorders.

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“…A first suggestion came from the neuronal cells' ability to use EA as a precursor of ACh. In chicken neuronal cultures, it was proved that EA is rapidly phosphorylated to phosphoethanolamine and converted to phosphatidylethanolamine that may also be methylated to phosphocholine (18). In vivo, intraventricular injections of 3 H-EA showed that the rat brain has the capacity to synthetize free choline de novo by stepwise methylation of EA, phosphoethanolamine and phosphatidylethanolamine (19).…”

Section: Oea Influences Cholinergic-mediated Food-reward Regulationmentioning

confidence: 99%

Ethanolamine Produced from Oleoylethanolamide Degradation Contributes to Acetylcholine/Dopamine Balance Modulating Eating Behavior

Mennella

Boudry

Val‐Laillet

2019

The Journal of Nutrition

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Oleoylethanolamide is a well-recognized anorectic compound which also has noteworthy effects on food-reward, influencing the acetylcholine (ACh)/dopamine (DA) balance in the cholinergic system. After its administration, oleoylethanolamide is quickly degraded into oleic acid and ethanolamine. The effect of oleic acid on the gut–brain axis has been extensively investigated, whereas ethanolamine has received scarce attention. However, there is scattered evidence from old and recent research that has underlined the influence of ethanolamine on the cholinergic system. In the present article, we propose a model by which the released ethanolamine contributes to the overall balance between DA and ACh after oleoylethanolamide administration.

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Uptake of ethanolamine in neuronal and glial cell cultures

Cited by 11 publications

References 10 publications

Effects of ethanolamine (ETN) Administration on etn and choline (CH) levels in plasma, brain extracellular fluid (ECF) and brain tissue, and on brain phospholipid levels in rats: An in vivo study

Effects of ethanolamine (ETN) Administration on etn and choline (CH) levels in plasma, brain extracellular fluid (ECF) and brain tissue, and on brain phospholipid levels in rats: An in vivo study

Influence of Myo-inositol Plus Ethanolamine on Plasmalogens and Cell Viability during Oxidative Stress

Ethanolamine Produced from Oleoylethanolamide Degradation Contributes to Acetylcholine/Dopamine Balance Modulating Eating Behavior

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