scholarly journals Lipoprotein size is a main determinant for the rate of hydrolysis by exogenous lipoprotein lipase in human plasma

2021 ◽  
pp. 100144
Author(s):  
Oleg Kovrov ◽  
Fredrik Landfors ◽  
Valeria Saar-Kovrov ◽  
Ulf Näslund ◽  
Gunilla Olivecrona
1982 ◽  
Vol 14 (2) ◽  
pp. 155-158 ◽  
Author(s):  
Yousry Gabr ◽  
Mohamedein Mahfouz ◽  
Esam Soliman ◽  
Farida Mansour

2019 ◽  
Vol 519 (1) ◽  
pp. 67-72 ◽  
Author(s):  
Mart Reimund ◽  
Anna Wolska ◽  
Robert Risti ◽  
Sierra Wilson ◽  
Denis Sviridov ◽  
...  

1993 ◽  
Vol 21 (3) ◽  
pp. 235S-235S ◽  
Author(s):  
BARBARA A. FIELDING ◽  
SANDY M. HUMPHREYS ◽  
KEITH N. FRAYN

1999 ◽  
Vol 32 (1) ◽  
pp. 15-23 ◽  
Author(s):  
Hiroshi Kimura ◽  
Yasuhiko Ohkaru ◽  
Koichi Katoh ◽  
Hiroo Ishii ◽  
Noriyuki Sunahara ◽  
...  

1982 ◽  
Vol 48 (03) ◽  
pp. 257-259 ◽  
Author(s):  
H R Lijnen ◽  
M Maes ◽  
M Castel ◽  
M Samama ◽  
D Collen

SummaryAcid-treated human plasma is a competitive inhibitor of the hydrolysis of D-Val-Leu-Lys-Nan (S-2251) by plasmin. The rate of hydrolysis is decreased to 50% by 750 fold diluted acidified normal plasma and by 60 fold diluted acidified α2-antiplasmin depleted plasma (α2-antiplasmin concentration less than 2%). These findings suggest that α2-antiplasmin is a contributary but not the main competitive inhibitor of acidified plasma. This interpretation is supported by the finding that α2-antiplasmin depleted plasma reconstituted with purified α2-antiplasmin inhibits the hydrolysis of S-2251 by plasmin at a 125 fold dilution following acidification and by the finding that in a purified system acid inactivated α2-antiplasmin inhibits the hydrolysis of S-2251 by plasmin with a Ki of 25 nM. Thus, besides α2-antiplasmin, other plasma proteins which are at least in part eliminated by the removal of α2-antiplasmin from plasma by immunoadsorption appear to be competitive inhibitors for plasmin in acidified plasma. It is suggested that several competitive inhibitors for plasmin are present and/or generated in acidified plasma and that these inhibitors may at least in part be responsible for the variability in the results of measurements of plasminogen and/or plasmin in plasma following acidification.


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