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Evidence for low molecular weight, non‐transferrin‐bound iron in rat brain and cerebrospinal fluid
Author(s) -
Moos Torben,
Morgan Evan H.
Publication year - 1998
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/(sici)1097-4547(19981115)54:4<486::aid-jnr6>3.0.co;2-i
Subject(s) - cerebrospinal fluid , transferrin , ferritin , chemistry , extracellular , endocytosis , antibody , extracellular fluid , receptor , biochemistry , endocrinology , microbiology and biotechnology , medicine , immunology , biology
Transferrin (Tf) donates iron (Fe) to the brain by means of receptor‐mediated endocytosis of Tf at the brain barriers. As Tf transport through the brain barriers is restricted, Fe is probably released into the brain extracellular compartment as non‐Tf‐bound iron (NTBI). To evaluate NTBI in the brain and cerebrospinal fluid (CSF), different aged rats (P15, P20, P56) were injected intravenously with [ 59 Fe‐ 125 I]Tf followed by sampling of CSF and brain tissue. Between 80 and 93% of 59 Fe in CSF was absorbed with anti‐Tf and 1 and 5% with anti‐ferritin antibodies. The fraction of 59 Fe from CSF passing through a 30,000 molecular weight (MW) cutoff filter was approximately 5% (P15), 10% (P20), and 15% (P56). Measurements of Fe and Tf concentrations in CSF of P20 rats revealed that the Fe‐binding capacity of Tf was exceeded. In the supernatants of brain homogenates, between 94 and 99% of 59 Fe was absorbed with anti‐Tf and anti‐ferritin antibodies. The respective fractions of 59 Fe in the supernatants passing through the 30 kD cutoff filter were 4% (P15), 2% (P20), and 6% (P56). In brain homogenates mixed before filtering with desferroxamine (DFO) or nitrilotriacetic acid (NTA) which complex loosely protein‐bound Fe and non‐protein‐bound Fe, these 59 Fe fractions were 2‐fold higher. The results indicate that NTBI is present extracellularly in CSF and probably in brain interstitium. J. Neurosci. Res. 54:486–494, 1998. © 1998 Wiley‐Liss, Inc.