Vanillin (3-methoxy-4-hydroxybenzaldehyde) inhibits mutation induced by hydrogen peroxide, N-methyl-N-nitrasoguanidine and mitomycin C but not Cs-137gamma-radiation at the CD59 locus in human-hamster hybrid A(L) cells

We have investigated the ability of the naturally occurring plant essence v anillin (3-methoxy-4-hydroxybenzaldehyde) to inhibit mutation at the CD59 l ocus on human chromosome 11 by hydrogen peroxide, N-methyl-N-nitrosoguanidi ne, mitomycin C and Cs-137 gamma-radiation in human-hamster hybrid AL cells . Previous studies using vanillin have suggested that it can inhibit chromo some aberrations induced by hydrogen peroxide and mitomycin C, as well as i nhibiting X-ray- and UV-induced mutations at the hprt locus. Other studies with vanillin have shown that it can increase both the toxicity and mutagen icity of ethyl methane sulfonate and increase the induction of sister chrom atid exchange by mitomycin C and a variety of other mutagens, The increased sensitivity of the AL assay, which is due in part to its ability to detect both small (single locus) and large (multilocus) genetic damage, allows us to measure the effect of vanillin at low doses of mutagen. Vanillin is sho wn, in these studies, to inhibit mutation induced by hydrogen peroxide, N-m ethyl-N-nitrosoguanidine and mitomycin C, as well as to enhance the toxicit y of these agents. Vanillin had no effect on either toxicity or mutation in duced by Cs-137 gamma-radiation. The vanillin-induced potentiation of H2O2 toxicity is shown not to involve inhibition of catalase or glutathione pero xidase, These results show that vanillin is able to inhibit mutation at the CD59 locus and modify toxicity in a mutagen-specific manner. Possible mech anisms to explain the action of vanillin include inhibition of a DNA repair process that leads to the death of potential mutants or enhancement of DNA repair pathways that protect from mutation but create lethal DNA lesions d uring the repair process.