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Subject: LUPUS/OXIDATION/FREE RADICAL

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   Biochem. Soc. Symp. 61: 1-31 (1995)[96232721]
   
Oxidative stress: the paradox of aerobic life.

   
   
    K. J. Davies
    
   
   
   Department of Biochemistry & Molecular Biology, Albany Medical
   College, NY 12208, USA.
   
   The paradox of aerobic life, or the 'Oxygen Paradox', is that higher
   eukaryotic aerobic organisms cannot exist without oxygen, yet oxygen
   is inherently dangerous to their existence. This 'dark side' of oxygen
   relates directly to the fact that each oxygen atom has one unpaired
   electron in its outer valence shell, and molecular oxygen has two
   unpaired electrons. Thus atomic oxygen is a free radical and molecular
   oxygen is a (free) bi-radical. Concerted tetravalent reduction of
   oxygen by the mitochondrial electron-transport chain, to produce
   water, is considered to be a relatively safe process; however, the
   univalent reduction of oxygen generates reactive intermediates. The
   reductive environment of the cellular milieu provides ample
   opportunities for oxygen to undergo unscheduled univalent reduction.
   Thus the superoxide anion radical, hydrogen peroxide and the extremely
   reactive hydroxyl radical are common products of life in an aerobic
   environment, and these agents appear to be responsible for oxygen
   toxicity. To survive in such an unfriendly oxygen environment, living
   organisms generate--or garner from their surroundings--a variety of
   water- and lipid-soluble antioxidant compounds. Additionally, a series
   of antioxidant enzymes, whose role is to intercept and inactivate
   reactive oxygen intermediates, is synthesized by all known aerobic
   organisms. Although extremely important, the antioxidant enzymes and
   compounds are not completely effective in preventing oxidative damage.
   To deal with the damage that does still occur, a series of damage
   removal/repair enzymes, for proteins, lipids and DNA, is synthesized.
   Finally, since oxidative stress levels may vary from time to time,
   organisms are able to adapt to such fluctuating stresses by inducing
   the synthesis of antioxidant enzymes and damage removal/repair
   enzymes. In a perfect world the story would end here; unfortunately,
   biology is seldom so precise. The reality appears to be that, despite
   the valiant antioxidant and repair mechanisms described above,
   oxidative damage remains an inescapable outcome of aerobic existence.
   In recent years oxidative stress has been implicated in a wide variety
   of degenerative processes, diseases and syndromes, including the
   following: mutagenesis, cell transformation and cancer;
   atherosclerosis, arteriosclerosis, heart attacks, strokes and
   ischaemia/reperfusion injury; chronic inflammatory diseases, such as
   rheumatoid arthritis, lupus erythematosus and psoriatic arthritis;
   acute inflammatory problems, such as wound healing; photo-oxidative
   stresses to the eye, such as cataract; central-nervous-system
   disorders, such as certain forms of familial amyotrophic lateral
   sclerosis, certain glutathione peroxidase-linked adolescent seizures,
   Parkinson's disease and Alzheimer's dementia; and a wide variety of
   age-related disorders, perhaps even including factors underlying the
   aging process itself. Some of these oxidation-linked diseases or
   disorders can be exacerbated, perhaps even initiated, by numerous
   environmental pro-oxidants and/or pro-oxidant drugs and foods.
   Alternatively, compounds found in certain foods may be able to
   significantly bolster biological resistance against oxidants.
   Currently, great interest centres on the possible protective value of
   a wide variety of plant-derived antioxidant compounds, particularly
   those from fruits and vegetables.
   
   MeSH Terms:
     * Antioxidants/metabolism
     * DNA Damage
     * Human
     * Oxidative Stress*
     * Oxygen/metabolism
     * Radioactive Pollutants
     * Reactive Oxygen Species
     * Superoxide Dismutase/metabolism
       
   
   
   Substances:
     * Oxygen
     * Reactive Oxygen Species
     * Radioactive Pollutants
     * Antioxidants
     * Superoxide Dismutase
       
   
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From 
Subject: LUPUS/OXIDATION/FREE RADICAL/COLLAGEN

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   Z Rheumatol 39: 84-90 (1980)[81035511]
   
Chromosomal instability in collagen disease.

   
   
    I. Emerit
    
   
   
   Chromosome instability is observed in patients with collagen disease.
   It is due to the presence of a chromosome-breaking agent in the serum
   which also induces chromosome breaks and rearrangements in blood
   cultures from healthy subjects. It is not possible to say at present
   whether this breakage factor is identical to that in patients with
   progressive systemic sclerosis, lupus erythematosus or rheumatoid
   arthritis. In all three diseases the agent is a substance with a low
   molecular weight between 1000 and 10,000 daltons. Since the enzyme
   superoxide dismutase has an anticlastogenic protective effect, the
   action of the agent on chromosomes is probably an indirect one, namely
   by generation of oxygen-dependent free radicals such as O2- x and OH.
   
   MeSH Terms:
     * Animal
     * Arthritis, Rheumatoid/physiopathology
     * Cells, Cultured
     * Chromosome Aberrations*
     * Collagen Diseases/physiopathology
     * Human
     * Lupus Erythematosus, Systemic/physiopathology
     * Mice
       
   
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