title: Mechanism of in vivo iron chelation by pyridoxal isonicotinoyl hydrazone and other imino derivatives of pyridoxal.
abstract: The source of iron chelated in vivo by the new iron-chelating agent PIH and its mechanism of excretion have been studied in normal and hypertransfused rats. PIH is able to chelate iron from both parenchymal and RE iron stores. Unlike DF, which promotes both urinary and fecal iron excretion, in this model PIH-induced iron excretion is limited almost entirely to the gut. Response to PIH is directly related to dosage, and oral doses ranging from 125 to 500 mg/kg/day are well tolerated. Six additional imino derivatives of pyridoxal have been studied, but none of these new compounds was as effective as PIH. Our study indicates that oral PIH is comparable in efficiency with parenteral DF and is of potential usefulness in the management of iron overload.
mesh_terms: D000818:Animals; D004305:Dose-Response Relationship, Drug; D005260:Female; D007501:Iron / Q000378:metabolism; D007502:Iron Chelating Agents / Q000378:metabolism / Q000494:pharmacology*; D007504:Iron Radioisotopes; D007538:Isoniazid / Q000008:administration & dosage / Q000031:analogs & derivatives* / Q000378:metabolism / Q000494:pharmacology; D011730:Pyridoxal / Q000008:administration & dosage / Q000031:analogs & derivatives* / Q000378:metabolism / Q000494:pharmacology; D051381:Rats
chemical_list: D007502:Iron Chelating Agents; D007504:Iron Radioisotopes; D011730:Pyridoxal; C021079:pyridoxal isonicotinoyl hydrazone; D007501:Iron; D007538:Isoniazid