Wookju Jang" /> Kyung-Hyun Cho*

" /> Wookju Jang, Nam Ho Jeoung, and Kyung-Hyun Cho*

" /> Wookju Jang, Nam Ho Jeoung, and Kyung-Hyun Cho*

. Mol. Cells 2011;31:461-70. https://doi.org/10.1007/s10059-011-1009-3">
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Mol. Cells 2011; 31(5): 461-470

Published online May 31, 2011

https://doi.org/10.1007/s10059-011-1009-3

© The Korean Society for Molecular and Cellular Biology

Modified Apolipoprotein (apo) A-I by Artificial Sweetener Causes Severe Premature Cellular Senescence and Atherosclerosis with Impairment of Functional and Structural Proper-ties of apoA-I in Lipid-Free and Lipid-Bound State

Wookju Jang1,4, Nam Ho Jeoung2,4, and Kyung-Hyun Cho1,3,*

1School of Biotechnology, Yeungnam University, Gyeongsan 712-749, Korea, 2Department of Fundamental Medical and Pharmaceutical Sciences, CU-Leaders College, Catholic University of Daegu, Gyeongsan 712-702, Korea, 3Research Institute of Protein Sensor, Yeungnam University, Gyeongsan 712-749, Korea, 4These authors contributed equally to this work.

Correspondence to : *Correspondence: chok@yu.ac.kr

Received: January 13, 2011; Revised: February 21, 2011; Accepted: March 3, 2011

Abstract

Long-term consumption of artificial sweeteners (AS) has been the recent focus of safety concerns. However, the potential risk of the AS in cardiovascular disease and lipoprotein metabolism has not been investigated sufficiently. We compared the influence of AS (aspartame, acesulfame K, and saccharin) and fructose in terms of functional and structural correlations of apolipoprotein (apo) A-I and high-density lipoproteins (HDL), which have atheroprotective effects. Long-term treatment of apoA-I with the sweetener at physiological concentration (3 mM for 168 h) resulted in loss of antioxidant and phospholipid binding activities with modification of secondary structure. The AS treated apoA-I exhibited proteolytic cleavage to produce 26 kDa-fragment. They showed pro-atherogenic properties in acetylated LDL phagocytosis of macrophages. Each sweetener alone or sweetener-treated apoA-I caused accelerated senescence in human dermal fibroblasts. These results suggest that long-term consumption of AS might accelerate atherosclerosis and senescence via impairment of function and structure of apoA-I and HDL.

Keywords apolipoprotein A-I, artificial sweetener, atherosclerosis, high-density lipoprotein, senescence

Article

Research Article

Mol. Cells 2011; 31(5): 461-470

Published online May 31, 2011 https://doi.org/10.1007/s10059-011-1009-3

Copyright © The Korean Society for Molecular and Cellular Biology.

Modified Apolipoprotein (apo) A-I by Artificial Sweetener Causes Severe Premature Cellular Senescence and Atherosclerosis with Impairment of Functional and Structural Proper-ties of apoA-I in Lipid-Free and Lipid-Bound State

Wookju Jang1,4, Nam Ho Jeoung2,4, and Kyung-Hyun Cho1,3,*

1School of Biotechnology, Yeungnam University, Gyeongsan 712-749, Korea, 2Department of Fundamental Medical and Pharmaceutical Sciences, CU-Leaders College, Catholic University of Daegu, Gyeongsan 712-702, Korea, 3Research Institute of Protein Sensor, Yeungnam University, Gyeongsan 712-749, Korea, 4These authors contributed equally to this work.

Correspondence to:*Correspondence: chok@yu.ac.kr

Received: January 13, 2011; Revised: February 21, 2011; Accepted: March 3, 2011

Abstract

Long-term consumption of artificial sweeteners (AS) has been the recent focus of safety concerns. However, the potential risk of the AS in cardiovascular disease and lipoprotein metabolism has not been investigated sufficiently. We compared the influence of AS (aspartame, acesulfame K, and saccharin) and fructose in terms of functional and structural correlations of apolipoprotein (apo) A-I and high-density lipoproteins (HDL), which have atheroprotective effects. Long-term treatment of apoA-I with the sweetener at physiological concentration (3 mM for 168 h) resulted in loss of antioxidant and phospholipid binding activities with modification of secondary structure. The AS treated apoA-I exhibited proteolytic cleavage to produce 26 kDa-fragment. They showed pro-atherogenic properties in acetylated LDL phagocytosis of macrophages. Each sweetener alone or sweetener-treated apoA-I caused accelerated senescence in human dermal fibroblasts. These results suggest that long-term consumption of AS might accelerate atherosclerosis and senescence via impairment of function and structure of apoA-I and HDL.

Keywords: apolipoprotein A-I, artificial sweetener, atherosclerosis, high-density lipoprotein, senescence

Mol. Cells
Nov 30, 2022 Vol.45 No.11, pp. 763~867
COVER PICTURE
Naive (cyan) and axotomized (magenta) retinal ganglion cell axons in Xenopus tropicalis (Choi et al., pp. 846-854).

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