Daily cocoa intake reduces the susceptibility of low-density lipoprotein to oxidation as demonstrated in healthy human volunteers

2001 ◽  
Vol 34 (1) ◽  
pp. 93-99 ◽  
Author(s):  
Naomi Osakabe ◽  
Seigo Baba ◽  
Akiko Yasuda ◽  
Tamami Iwamoto ◽  
Masumi Kamiyama ◽  
...  
2004 ◽  
Vol 50 (6) ◽  
pp. 679-684 ◽  
Author(s):  
Naomi Osakabe ◽  
Seigo Baba ◽  
Akiko Yasuda ◽  
Tamami Iwamoto ◽  
Masumi Kamiyama ◽  
...  

Author(s):  
Rojeet Shrestha ◽  
Shu-Ping Hui ◽  
Yusuke Miura ◽  
Akiko Yagi ◽  
Yuji Takahashi ◽  
...  

AbstractThe role of triglycerides carried in the triglyceride-rich lipoproteins (TRL) in the progression of atherosclerosis is uncertain. Identification of oxidized triglycerides and its possible association with atherosclerosis were largely ignored. Here we applied mass spectrometric approach to detect and identify triglyceride hydroperoxides (TGOOH) in human plasma and lipoproteins.EDTA plasma was collected from healthy human volunteers (n=9) after 14–16 h of fasting. Very low-density lipoprotein (VLDL)We identified 11 molecular species of TGOOH in either plasma or VLDL and IDL, of which TGOOH-18:1/18:2/16:0, TGOOH-18:1/18:1/16:0, TGOOH-16:0/18:2/16:0, TGOOH-18:1/18:1/18:1, and TGOOH-16:0/20:4/16:0 were most dominant. These TGOOH molecules are carried by TRL but not by LDL and HDL. Mean concentration of TGOOH in plasma, VLDL and IDL were, respectively, 56.1±25.6, 349.8±253.6 and 512.5±173.2 μmol/mol of triglycerides.This is the first report to identify several molecular species of oxidized triglycerides in TRL. Presence of oxidized triglyceride may contribute to the atherogenicity of TRL. Further work is needed to elucidate the association of the oxidized triglyceride in atherosclerosis.


1989 ◽  
Vol 80 (2) ◽  
pp. 101-109 ◽  
Author(s):  
Claude L. Malmendier ◽  
Jean-F. Lontie ◽  
Claude Delcroix ◽  
Thierry Magot

Author(s):  
Dean A. Handley ◽  
Cynthia M. Arbeeny ◽  
Larry D. Witte

Low density lipoproteins (LDL) are the major cholesterol carrying particles in the blood. Using cultured cells, it has been shown that LDL particles interact with specific surface receptors and are internalized via a coated pit-coated vesicle pathway for lysosomal catabolism. This (Pathway has been visualized using LDL labeled to ferritin or colloidal gold. It is now recognized that certain lysomotropic agents, such as chloroquine, inhibit lysosomal enzymes that degrade protein and cholesterol esters. By interrupting cholesterol ester hydrolysis, chloroquine treatment results in lysosomal accumulation of cholesterol esters from internalized LDL. Using LDL conjugated to colloidal gold, we have examined the ultrastructural effects of chloroquine on lipoprotein uptake by normal cultured fibroblasts.


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