Abstract
Administration of aflatoxin B1 (3 mg/kg body wt) to rats leads to strong inhibition of the acceptor activity of liver tRNA as measured by charging with [14C]-chorella protein hydrolysate. The maximum inhibition occurs 2 h after treatment. At increasing intervals after treatment, the inhibition appears to be gradually relieved, till control values are restored by 72 h. The charging experiment using several [14C]-amino acids separately shows pronounced inhibition of acceptor activity of all tRNA species, although the degree of inhibition varies with individual species. Preliminary results seem to rule out the possibility of hypermethylation of tRNA or damage to the CCA terminus as probable causes. The resultant functional changes may be attributed to a covalent interaction of aflatoxin B1-metabolite with tRNA.
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