RT info:eu-repo/semantics/article
T1 Nitric oxide-mediated mitochondrial impairment in neural cells: a role for glucose metabolism in neuroprotection
A1 Bolaños, Juan P.
A1 García-Nogales, Paula
A1 Vega-Agapito, Victoria
A1 Delgado-Esteban, María
A1 Cidad, Pilar
A1 Almeida, Angeles
AB Nitric oxide (žNO) is a highly diffusible, short-livedphysiological messenger present in the central nervoussystem (CNS) (Garthwaite et al., 1988) thatis synthesised by a family of nitric oxide synthases(NOSs) which catalyze the conversion of arginineto citrulline and žNO (Bredt and Snyder, 1990;Knowles and Moncada, 1994). All CNS cells synthesisežNO (Murphy et al., 1993). Neurones producežNO by calcium-dependent activation of neuronal,constitutive NOS (nNOS or NOS1), whereas glialcells synthesise žNO in a calcium-independent waythat requires previous transcriptional induction ofNOS (inducible NOS, iNOS or NOS2) (Galea et al.,1992; Simmons and Murphy, 1992). Astrocytes alsosynthesise žNO through NNOS activity (Murphy etal., 1990, 1991; Agullo´ andGarcı´a, 1992a,b). A thirdisoform of NOS (endothelial NOS, eNOS or NOS3)is associated with brain vasculature.In general, žNO participates in the transductionpathway leading to elevations in intracellular cyclicŁ Corresponding author: Dr. Juan P. Bolan˜os, Departamentode Bioquı´mica y Biologı´a Molecular, Universidadde Salamanca, Edificio Departamental, Plaza Doctoresde la Reina s=n, 37007 Salamanca, Spain. Tel.:C34-923-294526; Fax: C34-923-294579;E-mail: jbolanos@gugu.usal.esGMP levels (Bredt and Snyder, 1989; Knowles etal., 1989) and therefore participates in cyclic GMPfunctions (Wang and Robinson, 1997). However, anincreasing body of evidence is now arising to suggestthat žNO and its most active metabolite, the peroxynitriteanion (ONOO ), may be involved in the regulationof brain energy metabolism. This chapter willspecifically focus on the mechanisms involving žNOand ONOO -mediated interference with brain mitochondrialenergy production and the modulating roleof glutathione in cell energy metabolism. Finally, wediscuss recent evidence that strongly suggests theimportance of cell glucose utilisation in maintainingglutathione homeostasis and hence in preventingnitric oxide-mediated mitochondrial impairment.
PB Elsevier
YR 2001
FD 2001
LK https://uvadoc.uva.es/handle/10324/65607
UL https://uvadoc.uva.es/handle/10324/65607
LA eng
NO Progress in Brain Research
NO Producción Científica
DS UVaDOC
RD 23-nov-2024