Methylglyoxal induces nuclear accumulation of p53 and γH2AX in normal and cancer cells

The formation and accumulation of methylglyoxal (MGO) is associated with age-related diseases such as diabetes, cancer and neurodegenerative disorders. MGO is the major precursor of non-enzymatic glycation of macromolecules affecting their function and structure. We now show for the first time that MGO stress not only led to cellular aging responses like DNA double-strand breaks indicated by an accumulation of γH2AX in the nucleus. We also observed an immediate increase of Ser15 phosphorylated p53 in the nucleus of MGO treated cell lines which will change the cellular expression pattern with adverse effects on the cell cycle and other cellular functions not necessarily related to aging.