Adaptive changes in membrane lipid composition and fluidity as the basis for ethanol tolerance

Littleton, J M

doi:10.1016/0376-8716(79)90066-8

Cited by 10 publications

(4 citation statements)

References 15 publications

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“…The damaged glial cell population may suffer from poorer membrane stability that manifests as enhanced turnover of the Cho‐containing membrane constituents. This view finds support from studies that report such stability alterations after long‐term exposure to alcohol both in humans (Chin, 1977; Lee et al, 1980) and in rats (Grieve et al, 1979; Littleton, 1979). Our data do not show a decrease in the neuronal marker NAA and thus do not lend support to the neuronal hypothesis.…”

Section: Discussionmentioning

confidence: 54%

Brain Metabolic Alterations in Adolescents and Young Adults With Fetal Alcohol Spectrum Disorders

Fagerlund

Heikkinen

Autti‐Rämö

et al. 2006

Alcoholism Clin & Exp Res

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Section: Discussionmentioning

confidence: 54%

Brain Metabolic Alterations in Adolescents and Young Adults With Fetal Alcohol Spectrum Disorders

Fagerlund

Heikkinen

Autti‐Rämö

et al. 2006

Alcoholism Clin & Exp Res

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“…Ethanol causes a widely observed increase in membrane fluidity. − One of the regulatory pathways for membrane fluidity is the conversion of saturated fatty acids to unsaturated fatty acids through the activity of stearoyl-CoA desaturase. Our data set shows stearoyl-CoA desaturase has a statistically significant increase in protein expression and a fold change of 6.32 ± 0.03.…”

Section: Resultsmentioning

confidence: 99%

Quantitative Proteomic Characterization of Ethanol-Responsive Pathways in Rat Microglial Cells

Bell-Temin

Zhang²,

Chaput

et al. 2013

J. Proteome Res.

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Long-term exposure to alcohol can have profound effects on the central nervous system including pathophysiological consequences associated with neuroinflammation. Along with astroglia, microglia play an important role in the neuroinflammatory response. Using a SILAC-labeled rat microglial cell line, an expression profile of 2994 proteins was identified in ethanol-treated microglial cells, where 160 and 69 protein groups were determined to be significantly upregulated and downregulated, respectively. In addition, SILAC-based proteomic analysis of lipopolysaccharide-treated microglial cells was performed in order to generate a reference data set representing a "classical" (M1) macrophage activation response in order to compare to the differential protein expression profile of ethanol-treated microglia. On the basis of this comparison as well as other validation experiments performed in this study, ethanol appears to induce partial activation of microglia that is devoid of conventional markers that indicate an M1 phenotype. This study is the first comprehensive proteomic analysis to assess the impact of acute ethanol exposure on microglial function and will provide a significant foundation that includes novel protein markers for future work aimed to characterize the molecular mechanisms associated with ethanol-induced microglial activation and its role in neurodegeneration.

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“…An initial significant increase of Cho/NAA observed from the alcoholic group after 16 weeks exposure is probably due to the increased turnover of phosphatidylcholine and other phospholipids reflecting the adaptive mechanism of the brain in opposing the effect of chronic alcohol consumption (16). Rat studies, demonstrating an increase in fluidity of membrane (decrease in viscosity) after acute or short‐term exposure to alcohol, also have found that chronic alcohol exposure leads to membrane adaptation (17, 18) to minimize the fluidizing influence of alcohol. This change of membrane perturbation is in part responsible for the changes in membrane permeability and reduced/changed membrane protein activities affecting membrane transport required for normal cell functions.…”

Section: Discussionmentioning

confidence: 97%

Proton MR spectroscopic studies of chronic alcohol exposure on the rat brain

Lee

Holburn

Price

2003

Magnetic Resonance Imaging

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Purpose: To better understand the long-term pathophysiologic mechanisms of alcoholism-related organic brain damage by serially assessing brain metabolites in chronically exposed rats using both in vivo magnetic resonance spectroscopy (MRS) and high-resolution nuclear magnetic resonance (NMR) from brain extracts. Materials and Methods:The alcoholic regimen was continued up to 60 weeks. In vivo proton MRS studies were performed at 200 MHz using a small animal imaging/spectrometer. In vitro rat brain extracts were also examined using a 500 MHz vertical bore magnet. Comparison measurements were also obtained in an age-matched control group. Results:In vivo results showed that there is a significant increase in the Cho/NAA ratio in the chronic alcohol-exposed group that reached a maximum around 16 weeks. After 44 weeks of alcohol exposure, Cho/NAA in the alcohol group decreased significantly from its maximum value to a value that was significantly lower than those from the control groups. Brain extract studies demonstrated that PC and GPC were the main components responsible for the observed in vivo spectral changes after 16 and 60 weeks of alcohol consumption, respectively. Conclusion:The fluctuation of choline-containing metabolites during alcohol intoxication could explain sometimes seemingly conflicting and confusing results from MRS studies in human and animal studies in which the duration of alcohol consumption and amount are varied widely.

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Adaptive changes in membrane lipid composition and fluidity as the basis for ethanol tolerance

Cited by 10 publications

References 15 publications

Brain Metabolic Alterations in Adolescents and Young Adults With Fetal Alcohol Spectrum Disorders

Brain Metabolic Alterations in Adolescents and Young Adults With Fetal Alcohol Spectrum Disorders

Quantitative Proteomic Characterization of Ethanol-Responsive Pathways in Rat Microglial Cells

Proton MR spectroscopic studies of chronic alcohol exposure on the rat brain

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