Effect of methylglyoxal and advanced glycation end products on mitochondrial dynamics and physiology in astroglioma cells

VIVIANE GLASER; FILIPE JOSÉ DE MATOS; LILIANA SOSA; JESSICA FLORES; ALINE PERTILE REMOR; ANA JULIA VIEIRA; THIAGO LENOIR DA SILVA; ANA LUCIA DE PAUL; SUSANA GENTI-RAIMONDI; ALEXANDRA LATINI

Portugal

Simposio; Cell Symposia Mitochondria: from Signalling to Disease; 2013

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Chronic hyperglycemia, characteristics of diabetes mellitus (DM), appears to activate pathways implicated in the pathogenesis of DM complications, including methylglyoxal (MG) and advanced glycation end products (AGEs) formation. Here, the effect of MG (30-300uM) and AGEs (0.1-1mg/mL) on mitochondrial dynamics and physiology was studied in astroglioma cell culture (C6 cells). The content of mitochondrial fission (Drp1) and fusion (Mfn1) related proteins was analyzed by flow cytometry. Electron microscopy was used to observe mitochondrial content and morphometry. Oxygen consumption was assessed by high-resolution respirometry. AGEs exposure provoked increased content of mitochondria with smaller area, while Drp1 or Mfn2 content was unchanged, suggesting that Drp1 translocates to mitochondria, for inducing mitochondrial fission. Furthermore, increased basal respiration and state-IV, and lost of the respiratory control was induced by MG. Finally, MG and AGEs disrupted mitochondrial membrane potential. The data suggest that MG/AGEs induced mitochondrial impairment might be involved in the pathophysiology of DM complications.