Nitric oxide-mediated mitochondrial damage: A potential neuroprotective role for glutathione

Complex I assembly into supercomplexes determines differential mitochondrial ROS production in neurons and astrocytes

“…The status of many major redox couples in the brain is also regulated by astrocytes (9), through their high content of antioxidant compounds and enzymes (10) and by the constitutive stabilization of the master antioxidant transcriptional activator, nuclear factor erythroid 2-related factor 2 (Nrf2) (11). Thus, astrocytes are equipped to protect themselves when exposed to excess reactive oxygen species (ROS) (12) and reactive nitrogen species (13,14). Moreover, astrocytes also provide nearby neurons with protective antioxidant precursors through a cell-signaling mechanism involving glutamate receptor activation by neurotransmission (11,15,16).…”

Manipulación del transporte y consumo de oxígeno en la sepsis

“…Varios mecanismos participan en la génesis de la disfunción mitocondrial en la sepsis, entre estos destacan: 1) Reducción en la disponibilidad de sustratos como piruvato por bloqueo de la piruvato deshidrogenasa 55,56 , o de NADH por consumo por parte de la enzima poli (ADP-ribosa) polimerasa (PARP-1) 57,58 ; 2) Inhibición directa de los complejos de la cadena de fosforilación oxidativa secundaria a stress oxidativo 43,59,60 ; 3) Disminución en el contenido celular mitocondrial 46 ; 4) Aumento en la permeabilidad mitocondrial, ya sea por aumento en la expresión de proteínas desacopladoras o del poro de transición de permeabilidad mitocondrial, ambos fenómenos que se asocian a pérdida del gradiente mitocondrial, caída en la síntesis de ATP y activación de vías de apoptosis.…”

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“…Recently, our group demonstrated that treatment of mixed cell cultures with 10 µM Aβ (25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35) for 12 h and 24 h reduces SAT1 protein level as demonstrated by immunocytochemical and quantitative immunoreactivity analysis 20 . We now report the effects of Aβ(25-35) on SAT1 expression in rat cortical primary cell cultures.…”

“…A small 11-amino acid fragment of the fulllength peptide, Aβ (25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35), is a convenient alternative in Alzheimer's disease investigations as the peptide mimics several toxicological and oxidative stress properties of the native full-length peptide 4,18,19 . Recently, our group demonstrated that treatment of mixed cell cultures with 10 µM Aβ (25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35) for 12 h and 24 h reduces SAT1 protein level as demonstrated by immunocytochemical and quantitative immunoreactivity analysis 20 .…”