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Cytoprotective role of astaxanthin against glycated protein/iron chelate‐induced toxicity in human umbilical vein endothelial cells
Author(s) -
Nishigaki Ikuo,
Rajendran Peramaiyan,
Venugopal Ramachandran,
Ekambaram Gnapathy,
Sakthisekaran Dhanapal,
Nishigaki Yutaka
Publication year - 2010
Publication title -
phytotherapy research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.019
H-Index - 129
eISSN - 1099-1573
pISSN - 0951-418X
DOI - 10.1002/ptr.2867
Subject(s) - umbilical vein , antioxidant , lipid peroxidation , chemistry , biochemistry , toxicity , oxidative stress , enzyme , pharmacology , biology , in vitro , organic chemistry
Astaxanthin (ASX), a red carotenoid pigment with no pro‐vitamin A activity, is a biological antioxidant that occurs naturally in a wide variety of plants, algae and seafoods. This study investigated whether ASX could inhibit glycated protein/iron chelate‐induced toxicity in human umbilical‐vein endothelial cells (HUVEC) by interfering with ROS generation in these cells. Glycated fetal bovine serum (GFBS) was prepared by incubating fetal bovine serum (FBS) with high‐concentration glucose. Stimulation of cultured HUVECs with 50 m m 1 mL of GFBS significantly enhanced lipid peroxidation and decreased antioxidant enzyme activities and levels of phase II enzymes. However, preincubation of the cultures with ASX resulted in a marked decrease in the level of lipid peroxide (LPO) and an increase in the levels of antioxidant enzymes in an ASX concentration‐dependent manner. These results demonstrate that ASX could inhibit LPO formation and enhance the antioxidant enzyme status in GFBS/iron chelate‐exposed endothelial cells by suppressing ROS generation, thereby limiting the effects of the AGE–RAGE interaction. The results indicate that ASX could have a beneficial role against glycated protein/iron chelate‐induced toxicity by preventing lipid and protein oxidation and increasing the activity of antioxidant enzymes. Copyright © 2009 John Wiley & Sons, Ltd.