Bilirubin Accumulation by the Rabbit Choroid Plexus in vitro

Jakobson, Åke

doi:10.1159/000243412

Cited by 5 publications

(2 citation statements)

References 12 publications

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“…CHOROID PLEXUS EPITHELIUM Besides characteristic OAT-substrates, the choroid plexus has been shown to remove also larger and more lipophilic (i.e., more "bulky") organic anions from CSF such as iodipamide (Barany, 1973a,b), bile salts (Barany, 1974), and bilirubin (Jakobson, 1991). Choroid plexus transport of these organic anions was less sensitive to probenecid and not inhibitable by p-aminohippurate or urographic radiocontrast agents, but sensitive to a variety of organic compounds normally excreted into bile including bile salts, sulfobromophthalein (BSP) and cholegraphic contrast agents (Barany, 1973b).…”

Section: Polar Distribution Of Two Liver-like Organic Anion Transportmentioning

confidence: 99%

Organic anion transport across the choroid plexus

Gao

Meier

2000

Microsc. Res. Tech.

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Several organic anion transport systems have recently been identified and localized at the apical and basolateral plasma membrane domains of choroid plexus epithelial cells. These organic anion transporters include (1) indirectly coupled Na+/dicarboxylate cotransport and dicarboxylate/organic anion exchange, which is represented on the molecular level by a member of the “kidney”‐type organic anion transporter (OAT) family at the apical plasma membrane domain; (2) the organic anion transporting polypeptide 1 (Oatp1) and Oatp2, which both mediate typical “liver”‐like organic anion transport activities at the apical and basolateral plasma membrane domains, respectively; and (3) the multidrug resistance protein Mrp1/MRP1 at the basolateral plasma membrane domain, and the P‐glycoprotein Mdr1/MDR1 at an apical and subapical membrane vesicle compartment. This cellular transport polarity can account, at least in part, for the previously suggested physiologic transport properties of the choroid plexus epithelium and provides a framework for the identification and localization of additional organic anion transporters involved in the absorption and/or excretion of drugs and drug metabolites at the choroid plexus. Microsc. Res. Tech. 52:60–64, 2001. © 2001 Wiley‐Liss, Inc.

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Section: Polar Distribution Of Two Liver-like Organic Anion Transportmentioning

confidence: 99%

Organic anion transport across the choroid plexus

Gao

Meier

2000

Microsc. Res. Tech.

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“…No study has specifically investigated the involvement of MRP1 in UCB transport across the BCSFB. A considerable uptake of UCB by isolated rabbit CP has been described, which is inhibited by iodipamide, a substrate of organic anion transport systems (Jakobson, 1991). Which OATP or other transport proteins located at the brain-facing membranes of the BCSFB are involved in the clearance of UCB from the CNS remains an open question.…”

Section: Bilirubin Interactions With Metabolic/transport Processes Atmentioning

confidence: 99%

Transport and Metabolism at Blood–Brain Interfaces and in Neural Cells: Relevance to Bilirubin-Induced Encephalopathy

Gazzin¹,

Strazielle²,

Tiribelli³

et al. 2012

Front. Pharmacol.

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Bilirubin, the end-product of heme catabolism, circulates in non-pathological plasma mostly as a protein-bound species. When bilirubin concentration builds up, the free fraction of the molecule increases. Unbound bilirubin then diffuses across blood–brain interfaces (BBIs) into the brain, where it accumulates and exerts neurotoxic effects. In this classical view of bilirubin neurotoxicity, BBIs act merely as structural barriers impeding the penetration of the pigment-bound carrier protein, and neural cells are considered as passive targets of its toxicity. Yet, the role of BBIs in the occurrence of bilirubin encephalopathy appears more complex than being simple barriers to the diffusion of bilirubin, and neural cells such as astrocytes and neurons can play an active role in controlling the balance between the neuroprotective and neurotoxic effects of bilirubin. This article reviews the emerging in vivo and in vitro data showing that transport and metabolic detoxification mechanisms at the blood–brain and blood–cerebrospinal fluid barriers may modulate bilirubin flux across both cellular interfaces, and that these protective functions can be affected in chronic unconjugated hyperbilirubinemia. Then the in vivo and in vitro arguments in favor of the physiological antioxidant function of intracerebral bilirubin are presented, as well as the potential role of transporters such as ABCC1 and metabolizing enzymes such as cytochromes P-450 in setting the cerebral cell- and structure-specific toxicity of bilirubin following hyperbilirubinemia. The relevance of these data to the pathophysiology of bilirubin-induced neurological diseases is discussed.

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Lopez‐Anaya

Unadkat

Calkins

et al. 1993

Pharmaceutical Research

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The brain tissue is an important target for anti-HIV drug therapy. Since the permeability of the blood-brain and blood-cerebrospinal fluid (CSF) barriers may differ between neonates and adults, we have determined the effect of age on the distribution of zidovudine (ZDV or azidothymidine) into the CSF in the macaque (M. nemestrina). Five newborn macaques were administered ZDV (iv bolus, 5 mg/kg) at various ages (2 days to 4 months). Both CSF (cisternal) and venous blood samples were obtained at approximately 60 and 90 min after drug administration. In another series of experiments, adult female macaques received ZDV as either an iv bolus (5 and 10 mg/kg) or an infusion for at least 12 hr. CSF (lumbar) and venous blood samples were obtained at approximately 60 and 90 min after iv bolus and at more than 12 hr after iv infusion. ZDV concentration in the CSF and the plasma samples was determined by high-performance liquid chromatography. The CSF/plasma concentration ratio of ZDV in the newborn and adult macaques, after iv bolus administration, was independent of time. In addition, no significant (P > 0.05) difference was observed in the pooled iv bolus ZDV CSF/plasma concentration ratio between the adult group (0.236 +/- 0.058) and the newborns (0.213 +/- 0.039). Moreover, the ZDV CSF/plasma concentration ratio in the adults and the newborns, after iv bolus administration, was found not to be significantly (P > 0.05) different from the ratio obtained at steady state in the adults (0.224 +/- 0.094). These data indicate that the distribution of ZDV into the CSF in macaque neonates and adults is similar.

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Bilirubin Accumulation by the Rabbit Choroid Plexus in vitro

Cited by 5 publications

References 12 publications

Organic anion transport across the choroid plexus

Organic anion transport across the choroid plexus

Transport and Metabolism at Blood–Brain Interfaces and in Neural Cells: Relevance to Bilirubin-Induced Encephalopathy

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