Oxygen radicals and hydrogen peroxide in rat brain mitochondria

FEBS Letters ◽  
1974 ◽  
Vol 45 (1-2) ◽  
pp. 92-95 ◽  
Author(s):  
M.Catia Sorgato ◽  
L. Sartorelli
Keyword(s):  
Hydrogen Peroxide ◽  
Rat Brain ◽  
Oxygen Radicals ◽  
Brain Mitochondria ◽  
Rat Brain Mitochondria

Respiratory Activity of Isolated Rat Brain Mitochondria following in vitro Exposure to Oxygen Radicals

1983 ◽  
Vol 3 (2) ◽  
pp. 207-214 ◽  
Author(s):  
Lars Hillered ◽  
Lars Ernster
Keyword(s):  
Xanthine Oxidase ◽  
Rat Brain ◽  
Oxygen Radicals ◽  
Respiratory Activity ◽  
Brain Mitochondria ◽  
Iron Chelate ◽  
Rat Brain Mitochondria ◽  
In Vitro Exposure ◽  
Isolated Rat

Respiratory activity of isolated rat brain mitochondria was measured following in vitro exposure to oxygen radicals. The radicals were generated by hypoxanthine and xanthine oxidase in the presence of a suitable iron chelate and caused a severe inhibition of respiration stimulated by phosphate plus ADP (with malate + glutamate as substrate). The damage could be prevented by catalase or high concentrations of mannitol, but not by superoxide dismutase. A similar effect was observed when hypoxanthine and xanthine oxidase were replaced by glucose and glucose oxidase or by hydrogen peroxide. Most of the findings indicate that the hydroxyl radical is the damaging agent. It is concluded that brain mitochondria exposed to oxygen radicals in vitro show an inhibition of respiratory activity similar to that reported by other investigators as occurring in mitochondria in vivo following transient cerebral ischemia. Therefore, oxygen radicals may contribute to this type of cell damage.

Acyl-CoA: sn-Glycerol-3-Phosphate O-Acyltransferase in Rat Brain Mitochondria and Microsomes

1982 ◽  
Vol 39 (1) ◽  
pp. 286-289 ◽  
Author(s):  
Susan M. Fitzpatrick ◽  
Giovanna Sorresso ◽  
Dipak Haldar
Keyword(s):  
Rat Brain ◽  
Brain Mitochondria ◽  
Rat Brain Mitochondria

scholarly journals The role of ADP in the modulation of the calcium-efflux pathway in rat brain mitochondria

1985 ◽  
Vol 225 (1) ◽  
pp. 41-49 ◽  
Author(s):  
J Vitorica ◽  
J Satrústegui
Keyword(s):  
Rat Brain ◽  
Binding Sites ◽  
Tricarboxylic Acid Cycle ◽  
Brain Mitochondria ◽  
Ruthenium Red ◽  
Calcium Efflux ◽  
Rat Brain Mitochondria ◽  
Pi Complex ◽  
Efflux Pathway

The role of ADP in the regulation of Ca2+ efflux in rat brain mitochondria was investigated. ADP was shown to inhibit Ruthenium-Red-insensitive H+- and Na+-dependent Ca2+-efflux rates if Pi was present, but had no effect in the absence of Pi. The primary effect of ADP is an inhibition of Pi efflux, and therefore it allows the formation of a matrix Ca2+-Pi complex at concentrations above 0.2 mM-Pi and 25 nmol of Ca2+/mg of protein, which maintains a constant free matrix Ca2+ concentration. ADP inhibition of Pi and Ca2+ efflux is nucleotide-specific, since in the presence of oligomycin and an inhibitor of adenylate kinase ATP does not substitute for ADP, is dependent on the amount of ADP present, and requires ADP concentrations in excess of the concentrations of translocase binding sites. Brain mitochondria incubated with 0.2 mM-Pi and ADP showed Ca2+-efflux rates dependent on Ca2+ loads at Ca2+ concentrations below those required for the formation of a Pi-Ca2+ complex, and behaved as perfect cytosolic buffers exclusively at high Ca2+ loads. The possible role of brain mitochondrial Ca2+ in the regulation of the tricarboxylic acid-cycle enzymes and in buffering cytosolic Ca2+ is discussed.

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