Please use this identifier to cite or link to this item: http://hdl.handle.net/10316/4852
Title: Glutamate-mediated inhibition of oxidative phosphorylation in cultured retinal cells
Authors: Rego, Ana Cristina 
Sancha Santos, Maria 
Oliveira, Catarina Resende 
Keywords: Glutamate; Mitochondria; NMDA receptor; Retinal cells
Issue Date: 1999
Citation: Neurochemistry International. 36:2 (1999) 159-166
Abstract: Glutamate is an excitotoxin responsible for causing neuronal damage associated with mitochondria dysfunction. We have analyzed the relationship between the mitochondrial respiratory rate, the membrane potential ([Delta][Psi]) and the activity of mitochondrial complexes in retinal cells in culture, used as neuronal models. Glutamate (10 [mu]M-10 mM) dose-dependently decreased the O2 consumption and the membrane potential. A linear correlation was found between these parameters, suggesting that the mitochondrial respiratory function was affected. Exposure to glutamate (100 [mu]M) for 10 min, in the absence of Mg2+, inhibited the activity of complex I (26.3%), complexes II/III (22.2%) and complex IV (26.7%). MK-801 ((+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]-cyclohepten-5,10-imine hydrogen maleate), a non-competitive antagonist of the NMDA (N-methyl--aspartate) receptors, completely reversed the effect exerted by 100 [mu]M glutamate at the level of complexes I, II/III and IV. These results suggest that NMDA receptor-mediated inhibition of mitochondrial respiratory chain complexes may be responsible for the alteration in the respiratory rate of chick retinal cells submitted to glutamate.
URI: http://hdl.handle.net/10316/4852
DOI: 10.1016/S0197-0186(99)00107-2
Rights: openAccess
Appears in Collections:FMUC Medicina - Artigos em Revistas Internacionais

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