3H-amino acid incorporation into proteins during chronic aflatoxin induced coagulation defects in rabbits.
Eighteen New Zealand White rabbits were divided equally into three groups and administered either 0.2 ml dimethyl sulfoxide (DMSO)/day, 0.06 mg/kg/day Aflatoxin B1 (AFB1) in DMSO, or 0.09 mg/kg/day AFB1 in DMSO. Incorporation of 3H-amino acids into total serum protein, fibrinogen and platelet proteins was determined during the intoxication and developing coagulation defect. Ten of 18 rabbits administered AFB1 in DMSO died or developed prolonged coagulation times. There was no significant difference in specific incorporation of 3H-amino acids into total serum protein, fibrinogen or platelet proteins between groups, nor was there a difference in incorporation between rabbits with normal coagulation times and those with prolonged coagulation times. Correlation between plasma fibrinogen concentration and specific incorporation of 3H-amino acid into fibrinogen was not significant. In vivo inhibition of 3H-amino acid incorporation into plasma proteins or platelets could not be demonstrated.
D016604:Aflatoxin B1; D000596:Amino Acids / Q000378:metabolism*; D000818:Animals; D001778:Blood Coagulation Disorders / Q000139:chemically induced / Q000378:metabolism*; D005340:Fibrinogen / Q000096:biosynthesis; D008297:Male; D014176:Protein Biosynthesis; D011817:Rabbits; D014316:Tritium; D000096702:Aflatoxin Poisoning
D016604:Aflatoxin B1; D000596:Amino Acids; D005340:Fibrinogen; D014316:Tritium