Low density lipoprotein of synovial fluid in inflammatory joint disease is mildly oxidized

Lipids ◽  
1998 ◽  
Vol 33 (11) ◽  
pp. 1115-1121 ◽  
Author(s):  
M. J. James ◽  
D. van Reyk ◽  
K. A. Rye ◽  
R. T. Dean ◽  
L. G. Cleland ◽  
...  
1992 ◽  
Vol 83 (6) ◽  
pp. 657-664 ◽  
Author(s):  
K. Fairburn ◽  
M. Grootveld ◽  
R. J. Ward ◽  
C. Abiuka ◽  
M. Kus ◽  
...  

1. We have determined the antioxidant status of synovial fluid and serum of patients with inflammatory joint disease in terms of the biologically active lipid-soluble antioxidant, α-tocopherol. Synovial fluid concentrations of α-tocopherol were significantly lower relative to those of paired serum samples (P<0.001). Serum levels of α-tocopherol in these patients did not differ significantly from those in control serum. 2. Lower concentrations of cholesterol, triacylglycerol and low-density lipoprotein were also observed in patients' synovial fluid compared with matched serum samples. However, multiple regression analysis of the data indicated that there remained a significant depletion of α-tocopherol, which was largely independent of these co-variables, in inflammatory synovial fluid. These findings are consistent with the consumption of α-tocopherol within the inflamed joint via its role in terminating the process of lipid peroxidation. 3. Nuclear magnetic resonance spectroscopic analysis of matched inflammatory synovial fluid and serum confirmed lower concentrations of triacylglycerol in synovial fluid together with evidence of a shortened mean triacylglycerol chain length. The latter metabolic difference suggests an increased utilization of triacylglycerols for energy within the inflamed joint.


2000 ◽  
Vol 32 (6) ◽  
pp. 479-486 ◽  
Author(s):  
L. Dai ◽  
D.J. Lamb ◽  
D.S. Leake ◽  
M.L. Kus ◽  
H.W. Jones ◽  
...  

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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