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Hypoxanthine Transport and Metabolism in the Central Nervous System
Author(s) -
Spector Reynold
Publication year - 1988
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1988.tb03006.x
Subject(s) - hypoxanthine , inosine , choroid plexus , xanthine , purine , nucleotide , biochemistry , uric acid , chemistry , biology , adenosine , endocrinology , central nervous system , enzyme , gene
The mechanisms by which hypoxanthine, the principal purine in plasma and CSF, enters and leaves rabbit brain, choroid plexus, and CSF were investigated in the isolated choroid plexus in vitro and by injecting [ 14 C]hypo‐xanthine intraventricularly and [ 3 H]hypoxanthine intravenously. The isolated choroid plexus accumulated and extensively metabolized [ I4 C]hypoxanthine; however, l4 C was readily released from choroid plexus principally as [ I4 C]‐hypoxanthine. After infusion of [ 3 H]hypoxanthine intravenously, [ 3 H]hypoxanthine entered CSF and brain slowly and was converted in brain to nucleotides. Fewer than 5% of the acid‐soluble purine nucleotides in brain entered rabbit brain from plasma hypoxanthine (and inosine) per 24 h. After intraventricular injection of [ l4 C]hypoxanthine, the [ 14 C]hypoxanthine was cleared from the CSF into the blood or accumulated by brain and largely converted into 14 C‐nucleotides. Little [ 14 C]xanthine and no [ 14 C]uric acid or allantoin were formed. These studies show that brain, unlike most other tissues, rapidly recycles hypoxanthine and converts it into purine nucleotides, and not unsalvageable purines.Key Words: Blood‐brain barrier—Cerebrospinal fluid—Choroid plexus. Spector R. Hypoxanthine transport and metabolism in the central nervous system.