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The effects of green tea (–)‐epigallocatechin‐3‐gallate on reactive oxygen species in 3T3‐L1 preadipocytes and adipocytes depend on the glutathione and 67 kDa laminin receptor pathways
Author(s) -
Wang ChihTing,
Chang HsinHuei,
Hsiao ChiaoHsin,
Lee MengJung,
Ku HuiChen,
Hu YuJung,
Kao YungHsi
Publication year - 2009
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.200800013
Subject(s) - reactive oxygen species , glutathione , epigallocatechin gallate , catechin , chemistry , oxidative stress , adipocyte , receptor , biochemistry , adipose tissue , antioxidant , polyphenol , enzyme
Green tea (–)‐epigallocatechin‐3‐gallate (EGCG) is known as to regulate obesity and fat cell activity. However, little information is known about the effects of EGCG on oxidative reactive oxygen species (ROS) of fat cells. Using 3T3‐L1 preadipocytes and adipocytes, we found that EGCG increased ROS production in dose‐ and time‐dependent manners. The concentration of EGCG that increased ROS levels by 180–500% was approximately 50 μM for a range of 8–16 h of treatment. In contrast, EGCG dose‐ and time‐dependently decreased the amount of intracellular glutathione (GSH) levels. EGCG was more effective than (–)‐epicatechin, (–)‐epicatechin‐3‐gallate, and (–)‐epigallocatechin in changing ROS and GSH levels. This suggests a catechin‐specific effect. To further examine the relation of GSH to ROS as altered by EGCG, we observed that exposure of preadipocytes and adipocytes to N ‐acetyl‐ L ‐cysteine (a GSH precursor) blocked the EGCG‐induced increases in ROS levels and decreases in GSH levels. These observations suggest a GSH‐dependent effect of EGCG on ROS production. While EGCG was demonstrated to alter levels of ROS and GSH, its signaling was altered by an EGCG receptor (the so‐called 67 kDa laminin receptor(67LR)) antiserum, but not by normal rabbit serum. These data suggest that EGCG mediates GSH and ROS levels via the 67LR pathway.