Reduction of dopamine increases methylglyoxal-induced mitochondrial dysfunction in SH-SY5Y cells

As evidence for the roles of methylglyoxal in the development of diabetic neuropathy, oxidative stress and mitochondrial dysfunction play a key role in the mechanism of methylglyoxal-induced cell apoptosis. In this study, the results showed that dopamine can reduce the methylglyoxal-induced the oxidative stress and mitochondrial dysfunction in the SH-SY5Y cells. a-Methyl Tyrosine (MT) can inhibit the synthesis of dopamine, if SH-SY5Y cells was pre-incubated in the (MT), methylglyoxal-induced the oxidative stress and mitochondrial dysfunction was increased. One of PD symptoms is the reduction of the striatal DA content. In addition, the oxidative stress involving lipid peroxidation and mitochondrial dysfunction contributes to the pathogenesis of Parkinson’s Disease (PD). The results give one suggestion that methylglyoxal could enhance the processing the PD.