{'fraction_non_alphanumeric': 0.05767790262172284, 'fraction_numerical': 0.02247191011235955, 'mean_word_length': 5.242990654205608, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Pantothenic Acid Transport Through the Blood‐Brain Barrier

Abstract: The unidirectional influx of d‐pantothenic acid (PA) across cerebral capillaries, the anatomical locus of the blood‐brain barrier, was measured with an in situ rat brain perfusion technique using [3H]d‐PA (1.1 Ci/mmol). PA was transported across the blood‐brain barrier by a saturable system that could be described by a MichaelisMenten transport model with a half‐saturation concentration and maximal influx rate of 19 μM and 0.21 nmol/g of brain/min, respectively. PA (0.3 μM) transport through the blood‐brain barrier was significantly inhibited by probenecid, nonanoic acid, and biotin (all 0.25 mM), but not by penicillin G, pyruvate, β‐hydroxybutyrate. l‐leucine (all 1 mM), or poly‐l‐lysine HBr (1 mg/ml). Probenecid (0.25 mM), nonanoic acid (0.5 mM), and PA (1.0mM) did not inhibit [3H]l‐leucine transport through the blood‐brain barrier, whereas 30 μM‐l‐leucine inhibited [3H]leucine transport to 23% of control values. Thus, PA is transported through the blood‐brain barrier by a lowcapacity, saturable transport system with a half‐saturation concentration ‐10 times the plasma PA concentration. Although involved in the transfer of PA from blood into brain, this system does not play an important regulatory role in the synthesis of CoA from PA in brain.