ABSTRACT
Parkinson’s Disease (PD) is the most common neurodegenerative movement disorder produced in aged people. Several studies show that oxidative stress involving lipid peroxidation may contribute to the pathogenesis of PD (Yoshikawa, 1993). Recent studies have shown that diabetic patients with insulin resistant type 2 diabetes have a 23-180% increased risk for the development of PD (Hu et al., 2007). In individuals with short duration older-onset diabetes without complications have increased PD risk 103-617% (Driver et al., 2008). Methylglyoxal is known to be a toxic compound, and it is interesting that the toxicity of methylglyoxal is widely implicated in cell apoptosis. Diabetic neuropathy is a neurodegenerative condition comparable to Alzheimer’s disease. It includes many physiological mechanisms such as mitochondrial dysfunction, abnormal protein aggregation and inflammation (Picklo et al., 2002). Oxidative stress and mitochondrial dysfunction play a key role in the mechanism of methylglyoxal-induced cell apoptosis, which serves as an evidence for the roles of methylglyoxal and high glucose in the development of diabetic neuropathy (Di Loreto et al., 2008). Both the mitochondrial dysfunction and oxidative stress, either by increased production of ROS or impairments in the mechanism for scavenging ROS, could contribute to cell death in PD (Dawson and Dawson, 2003). In our study, the result showed that methylglyoxal increased the lipid peroxidation caused by oxidative stress and decreased the mitochondrial membrane potential in the SH-SY5Y cells. a-methyl tyrosine (MT) is a tyrosine hydroxylase inhibitor, inhibited the synthesis of dopamine. In our study, we show that if the SH-SY5Y cells was pre-incubated in MT for 24 h, methylglyoxal-induced the oxidative stress and mitochondrial dysfunction was increased, it was decreased by adding the dopamine. Our result suggests that results give one suggestion that methylglyoxal could enhance the processing the PD.
