The simplest to understand tRNA suppressors is to consider nonsense mutation (premature stop codon occuring in an ORF) generating a truncated translation product. Apart from reversion of the mutation, suppression of such mutation can also occur at the tRNA level: mutation in a tRNA(charged with an aa) generating a anticodon complementary to the stop codon will allow the loading of the amino acid specific of this tRNA when reading the stop codon. So this particular tRNA being in competition with the release factors to recognize the stop codon will allow the translation to continue beyond this premature stop codon and therefore the synthesis of the entire polypeptide, reversing the phenotype associated with the mutation though the mutation is still present in the ORF.
Considering Lys to Arg mutation : Lys codons are AAA and AAG and among Arg codons there are AGA and AGG. So a single substitution A to G in the codon is enough. Or one can consider a mutation in the anticodon of the Arg-tRNA allowing it to read AAA and AGA codons and therefore promoting Arg introduction when reading Lys codon.