Blood-brain barrier transport kinetics of the cyclic depsipeptide mycotoxins beauvericin and enniatins

2016 ◽  
Vol 258 ◽  
pp. 175-184 ◽  
Author(s):  
Lien Taevernier ◽  
Nathalie Bracke ◽  
Lieselotte Veryser ◽  
Evelien Wynendaele ◽  
Bert Gevaert ◽  
...  
Author(s):  
Nathalie Bracke ◽  
Yorick Janssens ◽  
Evelien Wynendaele ◽  
Liesa Tack ◽  
Alex Maes ◽  
...  

2016 ◽  
Vol 107 ◽  
pp. 460-470 ◽  
Author(s):  
Bert Gevaert ◽  
Evelien Wynendaele ◽  
Sofie Stalmans ◽  
Nathalie Bracke ◽  
Matthias D'Hondt ◽  
...  

Author(s):  
Lieselotte Veryser ◽  
Lien Taevernier ◽  
Tanmayee Joshi ◽  
Pratima Tatke ◽  
Evelien Wynendaele ◽  
...  

1991 ◽  
Vol 11 (5) ◽  
pp. 726-734 ◽  
Author(s):  
Doris J. Doudet ◽  
Catherine A. McLellan ◽  
Richard Carson ◽  
H. Richard Adams ◽  
Hitoshi Miyake ◽  
...  

Most attempts to model accurately [18F]-DOPA imaging of the dopamine system are based on the assumptions that its main peripheral metabolite, 3-O-methyl-6-[18F]fluoro-L-DOPA ([18F]3-OM-DOPA), crosses the blood-brain barrier but is present as a homogenous distribution throughout the brain, in part because it is not converted into [18F]DOPA in significant quantities. These assumptions were based mainly on data in rodents. Little information is available in the primate. To verify the accuracy of the above assumptions, we administered 18F-labeled 3-OM-DOPA to normal rhesus monkeys and animals with lesions of the DA nigrostriatal system. No selective 18F regional accumulation in brain was apparent in normal or lesioned animals. The plasma metabolite analysis revealed that only the negatively charged metabolites (e.g., sulfated conjugates) that do not cross the blood-brain barrier were found in significant quantities in the plasma. A one-compartment, three-parameter model was adequate to describe the kinetics of [18F]3-OM-DOPA. In conclusion, assumptions concerning [18F]3-OM-DOPA's behavior in brain appear acceptable for [18F]DOPA modeling purposes.


1987 ◽  
Vol 49 (5) ◽  
pp. 1651-1658 ◽  
Author(s):  
Quentin R. Smith ◽  
Seiji Momma ◽  
Masaki Aoyagi ◽  
Stanley I. Rapoport

1984 ◽  
Vol 247 (3) ◽  
pp. R582-R588 ◽  
Author(s):  
W. M. Pardridge ◽  
R. Sakiyama ◽  
G. Fierer

Lipophilic amine drugs such as propranolol and lidocaine are actively sequestered by tissues via saturable cytoplasmic binding systems. The present studies were designed to characterize the kinetics of drug transport and sequestration in rat brain in vivo by using the carotid injection technique. Both propranolol and lidocaine are sequestered by brain, and the half time (t 1/2) of clearance of the drugs from brain to blood is 6-7 min. The t 1/2 of propranolol association and dissociation reactions with the brain sequestration system are 0.38 +/- 0.03 and 1.33 +/- 0.20 min, respectively. The blood-brain barrier transport of propranolol and lidocaine is inhibited by acid pH, and drug transport is mediated by a low-affinity, high-capacity saturable transport system [propranolol half-saturation constant (Km) = 9.8 +/- 1.2 mM, maximal rate of saturable transport (Vmax) = 5.7 +/- 0.7 mumol X min-1 X g-1, and nonsaturable transport constant (KD) = 0.061 +/- 0.012 ml X min-1 X g-1). These studies indicate that in addition to cerebral blood flow, the distribution of lipophilic amines in brain is a function of plasma pH and of the activity of brain sequestration systems. The latter may represent high-capacity cytoplasmic drug-binding proteins that normally bind endogenous ligands in brain.


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