Ultrastructure of Reperf used Skeletal Muscle: The Effect of Oxygen Radical Scavenger Enzymes

1995 ◽  
Vol 15 (4) ◽  
pp. 155-162 ◽  
Author(s):  
K. Ytrehus ◽  
O. Reikerås ◽  
N. Huseby ◽  
R. Myklebust
Keyword(s):  
Skeletal Muscle ◽  
Oxygen Radical ◽  
Radical Scavenger ◽  
Effect Of Oxygen

Restoration of cerebrovascular responsiveness to hyperventilation by the oxygen radical scavenger n-acetylcysteine following experimental traumatic brain injury

1991 ◽  
Vol 75 (5) ◽  
pp. 774-779 ◽  
Author(s):  
Earl F. Ellis ◽  
Lyn Y. Dodson ◽  
Richard J. Police
Keyword(s):  
Free Radical ◽  
Brain Injury ◽  
Oxygen Free Radical ◽  
Oxygen Radical ◽  
Radical Scavenger ◽  
Content Type ◽  
Fluid Percussion ◽  
Experimental Traumatic Brain Injury ◽  
Experimental Fluid ◽  
Stimulation Of

✓ Previous experiments have shown that, following experimental fluid-percussion brain injury, cyclo-oxygenase-dependent formation of oxygen radicals prevents arteriolar vasoconstriction in response to hyperventilation. The oxygen radical scavengers superoxide dismutase and catalase restore normal reactivity; however, they are not routinely available for clinical use. The present study tested whether n-acetylcysteine (Mucomyst), an agent currently available for acetaminophen toxicity, could be used as a radical scavenger to restore reactivity after brain injury. N-acetylcysteine (163 mg/kg) was given intraperitoneally prior to or 30 minutes after fluid-percussion brain injury (2.6 atm) in cats, and reactivity to hyperventilation was tested 1 hour after injury. The authors found either that pre- or postinjury administration led to normal reactivity. Additional experiments supported the hypothesis that n-acetylcysteine is an oxygen radical scavenger, since it reduced or prevented the free radical-dependent cerebral arteriolar dilation normally induced by the topical application of arachidonic acid or bradykinin. The mechanism by which n-acetylcysteine is effective in trauma may involve direct scavenging of radicals or stimulation of glutathione peroxidase activity. The results suggest that n-acetylcysteine may be useful for treatment of oxygen free radical-mediated brain injury.

scholarly journals Use of Melatonin in Oxidative Stress Related Neonatal Diseases

Antioxidants ◽  
2020 ◽  
Vol 9 (6) ◽  
pp. 477
Author(s):  
Gabriella D’Angelo ◽  
Roberto Chimenz ◽  
Russel J. Reiter ◽  
Eloisa Gitto
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Defense ◽  
Perinatal Period ◽  
Oxygen Radical ◽  
Free Radical Scavenger ◽  
Radical Scavenger ◽  
Oxygen Species ◽  
Perinatal Brain Injury ◽  
Radical Generation ◽  
Prophylactic Use

Reactive oxygen species have a crucial role in the pathogenesis of perinatal diseases. Exposure to inflammation, infections, or high oxygen concentrations is frequent in preterm infants, who have high free iron levels that enhance toxic radical generation and diminish antioxidant defense. The peculiar susceptibility of newborns to oxidative stress supports the prophylactic use of melatonin in preventing or decreasing oxidative stress-mediated diseases. Melatonin, an effective direct free-radical scavenger, easily diffuses through biological membranes and exerts pleiotropic activity everywhere. Multiple investigations have assessed the effectiveness of melatonin to reduce the “oxygen radical diseases of newborn” including perinatal brain injury, sepsis, chronic lung disease (CLD), and necrotizing enterocolitis (NEC). Further studies are still awaited to test melatonin activity during perinatal period.

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