Concluding remarks: a prospective view of active oxygen in medicine

1982 ◽  
Vol 60 (11) ◽  
pp. 1425-1429 ◽  
Author(s):  
A. Petkau
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Free Radical ◽  
Active Oxygen ◽  
Radical Reactions ◽  
Free Radical Reactions ◽  
Free Radical Processes ◽  
Rational Therapy ◽  
The Central Nervous System ◽  
Radical Processes

Factors are identified that influence the initiation, propagation, and efficiency of free-radical processes, or that ameliorate or mask them. Major biochemical disruptions of the ischemic myocardium or the central nervous system are cited for their underlying free-radical reactions. Encouraging attempts at rational therapy of disease having a free-radical component are referenced.

Further studies on free-radical pathology in the major central nervous system disorders: effect of very high doses of methylprednisolone on the functional outcome, morphology, and chemistry of experimental spinal cord impact injury

1982 ◽  
Vol 60 (11) ◽  
pp. 1415-1424 ◽  
Author(s):  
H. B. Demopoulos ◽  
E. S. Flamm ◽  
M. L. Seligman ◽  
D. D. Pietronigro ◽  
J. Tomasula ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Central Nervous System ◽  
Nervous System ◽  
Free Radical ◽  
Tissue Injury ◽  
Functional Restoration ◽  
Radical Reactions ◽  
Free Radical Reactions ◽  
Cord Injury

The hypothesis that pathologic free-radical reactions are initiated and catalyzed in the major central nervous system (CNS) disorders has been further supported by the current acute spinal cord injury work that has demonstrated the appearance of specific, cholesterol free-radical oxidation products. The significance of these products is suggested by the fact that: (i) they increase with time after injury; (ii) their production is curtailed with a steroidal antioxidant; (iii) high antioxidant doses of the steroidal antioxidant which curtail the development of free-radical product prevent tissue degeneration and permit functional restoration. The role of pathologic free-radical reactions is also inferred from the loss of ascorbic acid, a principal CNS antioxidant, and of extractable cholesterol. These losses are also prevented by the steroidal antioxidant. This model system is among others in the CNS which offer distinctive opportunities to study, in vivo, the onset and progression of membrane damaging free-radical reactions within well-defined parameters of time, extent of tissue injury, correlation with changes in membrane enzymes, and correlation with readily measurable in vivo functions.

Highly stereocontrolled syntheses of 2,3-disubstituted 1,4-butyrolactones using ionic and free radical reactions

1993 ◽  
Vol 71 (9) ◽  
pp. 1407-1411 ◽  
Author(s):  
Stephen Hanessian ◽  
Benoit Vanasse ◽  
Hua Yang ◽  
Marco Alpegiani
Keyword(s):  
Free Radical ◽  
Radical Reactions ◽  
Substitution Reactions ◽  
Free Radical Reactions ◽  
Free Radical Processes ◽  
Radical Processes

N-Substituted 3-amino-1,4-butyrolactones undergo highly stereocontrolled substitution reactions via anionic and free radical processes.

scholarly journals Inflammation, Iron, Energy Failure, and Oxidative Stress in the Pathogenesis of Multiple Sclerosis

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Lukas Haider
Keyword(s):  
Oxidative Stress ◽  
Multiple Sclerosis ◽  
Central Nervous System ◽  
Nervous System ◽  
Free Radical ◽  
Free Radical Production ◽  
Mitochondrial Injury ◽  
Radical Production ◽  
The Central Nervous System ◽  
Energy Failure

Multiple sclerosis is a chronic inflammatory demyelinating disease of the central nervous system. Different trigger pathologies have been suggested by the primary cytodegenerative “inside-out” and primary inflammation-driven “outside-in” hypotheses. Recent data indicate that mitochondrial injury and subsequent energy failure are key factors in the induction of demyelination and neurodegeneration. The brain weighs only a few percent of the body mass but accounts for approximately 20% of the total basal oxygen consumption of mitochondria. Oxidative stress induces mitochondrial injury in patients with multiple sclerosis and energy failure in the central nervous system of susceptible individuals. The interconnected mechanisms responsible for free radical production in patients with multiple sclerosis are as follows: (i) inflammation-induced production of free radicals by activated immune cells, (ii) liberation of iron from the myelin sheets during demyelination, and (iii) mitochondrial injury and thus energy failure-related free radical production. In the present review, the different sources of oxidative stress and their relationships to patients with multiple sclerosis considering tissue injury mechanisms and clinical aspects have been discussed.

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