IBIMOL   23987
INSTITUTO DE BIOQUIMICA Y MEDICINA MOLECULAR PROFESOR ALBERTO BOVERIS
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Effects of ammonium on PC12 cells energy metabolism.
Autor/es:
KARADAYIAN, A.G.; BUSTAMANTE, J. ; ACOSTA, L.; LORES ARNAIZ, S.; RODRIGUEZ, L.
Lugar:
Villa Carlos Paz
Reunión:
Congreso; XXXIV Reunión Anual SAN 2019; 2019
Institución organizadora:
Sociedad Argentina de Neurociencias
Resumen:
Hyperammonaemia can induce deleterious effects on the CNS and many mechanisms have been proposed to explain its toxic effects. Such mechanisms include alteration in neurotransmission and interference with energy metabolism. Previous studies from our laboratory showed that in a model of hepatic encephalopathy, mitochondria were important targets of NH4+-toxicity. The aim of this work was to study if calcium mobilization could be a mediator of the suggested mitochondrial dysfunction. We exposed undifferentiated PC12 cells to 0.5, 1 and 2 mM NH4+/NH3 during 24 hs. After cell loading with Fluo4AM and TMRE, flow cytometry, plate reader, and fluorescence microscopy were employed to measure (Ca2+)c and mitochondrial membrane potential respectively. The results showed that PC12 cells exposure to all the NH3/NH4+ doses, decreases (Ca2+)c after 1 min KCl-depolarization for both methods employed. In addition, the results obtained for the lowest NH4+/NH3 dose (0.5 mM) by flow cytometry and plate reader showed an 85% and 75% decrease in the (Ca2+)c respectively. The calcium decrease after 0.5 mM NH4+/NH3 was accompanied by a 13% of mitochondrial hyperpolarization, as compared with untreated cells. We conclude that NH4+/NH3 with its consequent alkalinization, were not able to activate extracellular Ca2+ entry after KCl depolarization. Our findings may contribute to the understanding of pathologic ammonium effects in different brain cells, and to the treatment of hyperammonemia.