Lipid binding to sterol carrier protein-2 is inhibited by ethanol

Nicolai A. Avdulov; Svetlana V. Chochina; Urule Igbavboa; Christopher S. Warden; Friedhelm Schroeder; W. Gibson Wood

doi:10.1016/S0005-2760(98)00178-7

Lipid binding to sterol carrier protein-2 is inhibited by ethanol

Nicolai A. Avdulov, Svetlana V. Chochina, Urule Igbavboa, Christopher S. Warden, Friedhelm Schroeder, W. Gibson Wood

Research output: Contribution to journal › Article › peer-review

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Abstract

Sterol carrier an protein-2 (SCP-2) is intracellular lipid carrier protein that binds cholesterol, phospholipids, fatty acids and other ligands. It has been reported that expression of SCP-2 was increased in brain nerve endings or synaptosomes of chronic ethanol-treated mice and it was shown that cholesterol homeostasis was altered in brain membranes of chronic ethanol- treated animals. Ethanol may interfere with the capacity of SCP-2 to bind cholesterol as well as other lipids. This hypothesis was tested using recombinant SCP-2 and fluorescent-labeled cholesterol, phosphatidylcholine (PC), and stearic acid. The association constants (K(a)) of the ligand-SCP-2 complex were in the following order: NBD-cholesterol > NBD-PC > NBD- stearic acid. Ethanol, beginning at a concentration of 25 mM, significantly reduced the affinity of NBD-cholesterol and NBD-PC for SCP-2. Effects of ethanol on the K(a) of NBD-stearic acid was significant only at the highest concentration that was examined (200 mM). Ethanol significantly increased the B(max) of NBD-cholesterol for SCP-2 but did not have a significant effect on the B(max) of NBD-PC. Similar results were found for effects of ethanol on the K(a)s and B(max)s using pyrene-labeled cholesterol and PC. In conclusion, ethanol beginning at a physiological concentration of 25 mM inhibited binding of cholesterol and PC to SCP-2. However, effects of ethanol on lipid binding to SCP-2 were dependent on the type of lipid. Ethanol in vivo may interfere with lipid binding to SCP-2 and disrupt lipid trafficking within cells.

Original language	English (US)
Pages (from-to)	37-45
Number of pages	9
Journal	Biochimica et Biophysica Acta - Molecular and Cell Biology of Lipids
Volume	1437
Issue number	1
DOIs	https://doi.org/10.1016/S0005-2760(98)00178-7
State	Published - Jan 29 1999
Externally published	Yes

Bibliographical note

Funding Information:
This work was supported by NIH Grants AA10806 (to N.A.A.), AG11056 (to W.G.W.), GM 31651 (to F.S.) and the Medical Research Program of the Department of Veterans Affairs (W.G.W.).

Keywords

Brain
Cholesterol
Ethanol
Lipid
Lipid transport
Sterol carrier protein-2

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10.1016/S0005-2760(98)00178-7

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title = "Lipid binding to sterol carrier protein-2 is inhibited by ethanol",

abstract = "Sterol carrier an protein-2 (SCP-2) is intracellular lipid carrier protein that binds cholesterol, phospholipids, fatty acids and other ligands. It has been reported that expression of SCP-2 was increased in brain nerve endings or synaptosomes of chronic ethanol-treated mice and it was shown that cholesterol homeostasis was altered in brain membranes of chronic ethanol- treated animals. Ethanol may interfere with the capacity of SCP-2 to bind cholesterol as well as other lipids. This hypothesis was tested using recombinant SCP-2 and fluorescent-labeled cholesterol, phosphatidylcholine (PC), and stearic acid. The association constants (K(a)) of the ligand-SCP-2 complex were in the following order: NBD-cholesterol > NBD-PC > NBD- stearic acid. Ethanol, beginning at a concentration of 25 mM, significantly reduced the affinity of NBD-cholesterol and NBD-PC for SCP-2. Effects of ethanol on the K(a) of NBD-stearic acid was significant only at the highest concentration that was examined (200 mM). Ethanol significantly increased the B(max) of NBD-cholesterol for SCP-2 but did not have a significant effect on the B(max) of NBD-PC. Similar results were found for effects of ethanol on the K(a)s and B(max)s using pyrene-labeled cholesterol and PC. In conclusion, ethanol beginning at a physiological concentration of 25 mM inhibited binding of cholesterol and PC to SCP-2. However, effects of ethanol on lipid binding to SCP-2 were dependent on the type of lipid. Ethanol in vivo may interfere with lipid binding to SCP-2 and disrupt lipid trafficking within cells.",

keywords = "Brain, Cholesterol, Ethanol, Lipid, Lipid transport, Sterol carrier protein-2",

author = "Avdulov, {Nicolai A.} and Chochina, {Svetlana V.} and Urule Igbavboa and Warden, {Christopher S.} and Friedhelm Schroeder and Wood, {W. Gibson}",

note = "Funding Information: This work was supported by NIH Grants AA10806 (to N.A.A.), AG11056 (to W.G.W.), GM 31651 (to F.S.) and the Medical Research Program of the Department of Veterans Affairs (W.G.W.).",

year = "1999",

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doi = "10.1016/S0005-2760(98)00178-7",

language = "English (US)",

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T1 - Lipid binding to sterol carrier protein-2 is inhibited by ethanol

AU - Avdulov, Nicolai A.

AU - Chochina, Svetlana V.

AU - Igbavboa, Urule

AU - Warden, Christopher S.

AU - Schroeder, Friedhelm

AU - Wood, W. Gibson

N1 - Funding Information: This work was supported by NIH Grants AA10806 (to N.A.A.), AG11056 (to W.G.W.), GM 31651 (to F.S.) and the Medical Research Program of the Department of Veterans Affairs (W.G.W.).

PY - 1999/1/29

Y1 - 1999/1/29

N2 - Sterol carrier an protein-2 (SCP-2) is intracellular lipid carrier protein that binds cholesterol, phospholipids, fatty acids and other ligands. It has been reported that expression of SCP-2 was increased in brain nerve endings or synaptosomes of chronic ethanol-treated mice and it was shown that cholesterol homeostasis was altered in brain membranes of chronic ethanol- treated animals. Ethanol may interfere with the capacity of SCP-2 to bind cholesterol as well as other lipids. This hypothesis was tested using recombinant SCP-2 and fluorescent-labeled cholesterol, phosphatidylcholine (PC), and stearic acid. The association constants (K(a)) of the ligand-SCP-2 complex were in the following order: NBD-cholesterol > NBD-PC > NBD- stearic acid. Ethanol, beginning at a concentration of 25 mM, significantly reduced the affinity of NBD-cholesterol and NBD-PC for SCP-2. Effects of ethanol on the K(a) of NBD-stearic acid was significant only at the highest concentration that was examined (200 mM). Ethanol significantly increased the B(max) of NBD-cholesterol for SCP-2 but did not have a significant effect on the B(max) of NBD-PC. Similar results were found for effects of ethanol on the K(a)s and B(max)s using pyrene-labeled cholesterol and PC. In conclusion, ethanol beginning at a physiological concentration of 25 mM inhibited binding of cholesterol and PC to SCP-2. However, effects of ethanol on lipid binding to SCP-2 were dependent on the type of lipid. Ethanol in vivo may interfere with lipid binding to SCP-2 and disrupt lipid trafficking within cells.

AB - Sterol carrier an protein-2 (SCP-2) is intracellular lipid carrier protein that binds cholesterol, phospholipids, fatty acids and other ligands. It has been reported that expression of SCP-2 was increased in brain nerve endings or synaptosomes of chronic ethanol-treated mice and it was shown that cholesterol homeostasis was altered in brain membranes of chronic ethanol- treated animals. Ethanol may interfere with the capacity of SCP-2 to bind cholesterol as well as other lipids. This hypothesis was tested using recombinant SCP-2 and fluorescent-labeled cholesterol, phosphatidylcholine (PC), and stearic acid. The association constants (K(a)) of the ligand-SCP-2 complex were in the following order: NBD-cholesterol > NBD-PC > NBD- stearic acid. Ethanol, beginning at a concentration of 25 mM, significantly reduced the affinity of NBD-cholesterol and NBD-PC for SCP-2. Effects of ethanol on the K(a) of NBD-stearic acid was significant only at the highest concentration that was examined (200 mM). Ethanol significantly increased the B(max) of NBD-cholesterol for SCP-2 but did not have a significant effect on the B(max) of NBD-PC. Similar results were found for effects of ethanol on the K(a)s and B(max)s using pyrene-labeled cholesterol and PC. In conclusion, ethanol beginning at a physiological concentration of 25 mM inhibited binding of cholesterol and PC to SCP-2. However, effects of ethanol on lipid binding to SCP-2 were dependent on the type of lipid. Ethanol in vivo may interfere with lipid binding to SCP-2 and disrupt lipid trafficking within cells.

KW - Brain

KW - Cholesterol

KW - Ethanol

KW - Lipid

KW - Lipid transport

KW - Sterol carrier protein-2

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JO - Biochimica et Biophysica Acta - Molecular and Cell Biology of Lipids

JF - Biochimica et Biophysica Acta - Molecular and Cell Biology of Lipids

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ER -

Lipid binding to sterol carrier protein-2 is inhibited by ethanol

Abstract

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