The effects of methylglyoxal on the mitochondria

The mitochondrion is the cellular “powerhouse” and the integrity of its bioenergetic function is essential in survival. This role is fulfilled by mainly oxidizing NADH+H+ and pyruvate produced essentially in cytosolic glycolysis, inevitably forming toxic methylglyoxal (MGO). The production of cellular energy currency is linked to the function of respiratory chain using molecular oxygen as final electron acceptor and being the source of reactive oxygen species (ROS) formation, too. Although, the cells are well-equipped with protective mechanisms against MGO, the insufficiency of defense system results in the attack to cellular compartments. Mitochondrion is a target of such an insult and the thus emerging mitochondrial dysfunction involves respiratory chain inhibition parallel to ROS formation, protein glycation, lipid peroxidation, and mitochondrial membrane destruction concomitant with dissipation of mitochondrial membrane potential. These pathophysiological changes lead to mitochondrion-dependent cell apoptosis. However, to unmask the molecular mechanisms underlying MGO-induced apoptosis, further studies are needed.