Dopamine modifies oxygen consumption and mitochondrial membrane potential in striatal mitochondria
- 138 Downloads
Dopamine is a neurotransmitter that has been related to mitochondrial dysfunction. In this study, striatal intact mitochondria and submitochondrial membranes were incubated with different dopamine concentrations, and changes on mitochondrial function, hydrogen peroxide, and nitric oxide production were evaluated. A 35% decrease in state 3 oxygen uptake (active respiration state) was found after 1 mM dopamine incubation. In addition, mitochondrial respiratory control significantly decreased, indicating mitochondrial dysfunction. High dopamine concentrations induced mitochondrial depolarization. Also, evaluation of hydrogen peroxide production by intact striatal mitochondria showed a significant increase after 0.5 and 1 mM dopamine incubation. Incubation with 0.5 and 1 mM dopamine increased nitric oxide production in submitochondrial membranes by 28 and 49%, respectively, as compared with control values. This study provides evidence that high dopamine concentrations induce striatal mitochondrial dysfunction through a decrease in mitochondrial respiratory control and loss of membrane potential, probably mediated by free radical production.
KeywordsStriatal mitochondria Dopamine Membrane potential
This research was supported by grants from Universidad de Buenos Aires, Consejo Nacional de Investigaciones Científicas y Técnicas and Agencia Nacional de Promoción Científica y Tecnológica, Argentina.
- 3.Murphy A (2000) Mitochondria in human disease. The Biochemist 22:19–24Google Scholar
- 11.Khan FH, Sen T, Maiti AK, Jana S, Chatterjee U, Chakrabarti S (2005) Inhibition of rat brain mitochondrial electron transport chain activity by dopamine oxidation products during extended in vitro incubation: implications for Parkinson’s disease. Biochim Biophys Acta 1741(1–2):65–74PubMedGoogle Scholar
- 20.Jana S, Maiti AK, Bagh MB, Banerjee K, Das A, Roy A, Chakrabarti S (2007) Dopamine but not 3, 4-dihydroxy phenylacetic acid (DOPAC) inhibits brain respiratory chain activity by autoxidation and mitochondria catalyzed oxidation to quinone products: implications in Parkinson’s disease. Brain Res 1139:195–200CrossRefPubMedGoogle Scholar
- 21.Boveris A (1998) Regulation of mitochondrial respiration by ADP, O2 and NO. Medicina (B Aires) 58(5 Pt 2):559–560Google Scholar