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Urinary excretion of µ‐aminopropionitrile and cyanoacetic acid
Author(s) -
Fleisher Joseph H.,
Peacock Erle E.,
Chvapil Milos
Publication year - 1978
Publication title -
clinical pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.941
H-Index - 188
eISSN - 1532-6535
pISSN - 0009-9236
DOI - 10.1002/cpt1978235520
Subject(s) - cyanoacetic acid , urine , urinary system , excretion , metabolite , medicine , chemistry , endocrinology , biochemistry
Human serum did not convert µ‐aminopropionitrile (BAPN) to the deaminated, nonlathyrogenic metabolite, cyanoacetic acid (CAA). Instead, its enzymic activity for oxidizing benzylamine was inhibited by BAPN (I 50 = 2 × 10 −3 M). BAPN was found in the urine within one hour of oral administration. Oral 250 mg BAPN at 6‐hr intervals each day for 21 days resulted in urinary BAPN recoveries approximating 16% of the total dose. BAPN was not detected in urine in specimens collected later than 7 hr after cessation of BAPN dosage. Urinary CAA appeared more slowly than BAPN and increased gradually to approximately three times that of urinary BAPN. After BAPN was discontinued, there was prolonged urinary excretion of BAPN‐derived CAA. These along with earlier findings in experimental animals suggest that unexcreted BAPN is sequestered in tissues where it is metabolized to CAA before being slowly released.