Cytotoxicity of 3-Hydroxykynurenine: Implications for CNS Damage in Neonatal Vitamin B-6 Deficiency
Pyridoxal phosphate, the biologically active form of vitamin B-6, plays a central role in the metabolism of amino acids and biogenic amines. A deficiency of this vitamin in human infants or in neonates of various species results in a deficiency syndrom characterized by marked neurological impairment (Coursin, 1969). The neurological deficits associated with neonatal vitamin B-6 deficiency include ataxia, irritability, tremor and seizures (Coursin, 1969). CNS histopathological changes resulting from neonatal vitamin B-6 deficiency have not been extensively studied. However, several investigators have reported neuropathological alterations suggestive of impaired development, neuronal loss or damage, or premature aging of CNS neurons (Morre et al., 1978; Root and Longenecker, 1983; Wasynczuk et al., 1983).
KeywordsQuinolinic Acid Kynurenine Pathway Pyridoxal Phosphate Hybrid Cell Line Quinone Imine
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