The tumour suppressor gene p53 encodes a protein whose major function is to protect the organism from the proliferation of potentially tumorigenic cells. Seventy per cent of the lung cancers display a mutation in the p53 gene. Statistical studies show the existence of a significant correlation between this high amount of p53 mutation and the tobacco smoking habits of the patients. A high level of p53 gene mutation occurs frequently at amina acid residues 157, 248 and 273. Biochemical studies show that corresponding codons are preferred targets for the metabolites derived from B[a]P Hypothesizing that the search for mutation in p53 gene expressed in eukaryotic cells would lead to a better evaluation of the mutagenic capacity of tobacco smoke in human, we developed a assay based on the expression of p53 gene in Sacchamyces cerevisae . The strain devoted to the assay was constructed by integrating one copy of the human p53 gene in the yeast genome and introducing several copies of a suicide gene placed under the control of wt-p53 protein, in each cell. CAN1 was selected as suicide gene. Its expression in presence of the L-canavanine leads to cell death. We showed that, in low toxicity conditions, this yeast strain allows to identify the mutagenic capacity of the gaseous-phase of tobacco smoke. We confirmed that the surviving of yeast in the presence of L-canavanine is actually determined by the acquisition of a mutation or a deletion in the p53 gene. We characterized several p53 mutations and showed that some of them correspond to those expected following a exposure to B[a]P.