Aminoacetone (AA) is a threonine and glycine catabolite long-known to accumulate in cri-du-chat and threoninemia. More recently, threonine was pointed out as an endogenous source of methylglyoxal (MG), contributing, together with triose phosphates and acetone, to the symptoms of diabetes mellitus. Although the metabolic function of AA has not been clarified yet, it is known that the AA enzymatic ("semicarbazide sensitive amino oxidase")-or the metal (Cu²⁺ or Fe²⁺ ions)-catalyzed oxidation product, MG, inhibit angiogenesis in diabetics. Considering that MG is reported to trigger apoptosis and/or necrosis in insulin-producing cells (RINm5f) and that the chemical oxidation of AA is propagated by superoxide anion radical, here we propose to study a possible pro-oxidant role of AA in pancreatic β-cells´ death. RINm5f cells were seeded in 200 mL culture medium in 96-well microplates (10⁴ cells/well) and allowed to attach to the plates for 48 h before the addition of 0.1-10.0 mM AA. Cytotoxicity was monitored by the MTT assay at 6 and 24 h after AA treatment. Addition of the enzymatic and chemical antioxidants catalase (1.0-5.0 mM), superoxide dismutase (5-50 U/mL), semicarbazide (0,5 – 5 mM) and N-acetylcystein (0,5 mM – 10,0 mM) to the plates is shown to provide partial protection to the RINm5f cells. Although the AA physiological concentrations have not yet been determined in the tissues of diabetics, the model studies described here support the hypothesis that AA overload may contribute to pancreatic β-cell death.