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with a free hand, but give only your own."
-- J.R.R.
Tolkien The Children of Hurin
- Peroxynitrites
-
General
Information:
Names:
Wikipedia entry:
Dr. Ray Shahelien entry:
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Observations:
It
turns out that the same toxin (peroxynitrite)
that probably causes damage to the brain in Alzheimer's
disease also
damages the brain as a result of a stroke.
http://www.jneurosci.org/content/19/14/5910.short
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1865248/
Various essential oils protect the brain in four ways: they
limit the formation of peroxynitrites, they lower levels of
peroxynitrites, they inhibit peroxynitrite-mediated damage,
and they
partially reverse the damage done by peroxynitrites. In
essence, they limit the damage done to the brain by stroke and
Alzheimer's disease.
See also"aromatherapy in the treatment
of Alzheimer's disease"
http://www.alzconnected.org/discussion.aspx?g=posts&t=2147484055
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Known
sources:
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Natural
sources:
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References:
Richardson:
Free
radicals
in the genesis of Alzheimer's disease
J. S. Richardson
Department of Pharmacology, College of
Medicine, University of Saskatchewan, Saskatoon, Canada.
"As
part of an ongoing investigation of the role of oxygen free
radicals
in Alzheimer's disease (AD), the formation of peroxidation
products,
the activities of free radical defense enzymes, and the level
of
total iron were determined in autopsy brain tissue from donors
with
AD and from age-matched non-demented donors."
[Is this the
"Dr. Richardson" cited by
http://www.consumerhealth.org/articles/display.cfm?ID=19990303140150
?
If so, they got his title wrong!]
[Seems as though
chelation therapy with EDTA depletes excess iron as well as
other
metals. Perhaps this is the reason why chelation
therapists
have noticed an improvement in their patients who suffer from
AD.
Aluminum might be, as someone put it, "an innocent
bystander".]
http://www.annalsnyas.org/cgi/content/abstract/695/1/73
[An interesting Google search on on-line articles
referencing the above. Hopefully the link works.]
http://scholar.google.com/scholar?q=link:http%3A%2F%2Fwww.annalsnyas.org%2Fcgi%2Fcontent%2Fabstract%2F695%2F1%2F73
[Other papers by Richardson]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Search&db=PubMed&term=Richardson+%22University+of+Saskatchewan%22+Alzheimer%27s&tool=QuerySuggestion
"Cerebral microischemia as a potential precipitant of the
neurodegenerative cascade of Alzheimer's disease."
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9329719&dopt=Abstract
Neuroprotection by
minocycline caused by direct and specific scavenging of
peroxynitrite.
Schildknecht S, Pape R, Müller N, Robotta M, Marquardt A,
Bürkle A, Drescher M, Leist M.
J
Biol Chem. 2011 Feb 18;286(7):4991-5002. Epub 2010 Nov 16.
Source:
Department of In Vitro Toxicology and Biomedicine, Faculty of
Biology, University of Konstanz, 78457 Konstanz, Germany.
Abstract
Minocycline prevents oxidative protein modifications and
damage in disease models associated with inflammatory glial
activation and oxidative stress. Although the drug has been
assumed to act by preventing the up-regulation of
proinflammatory enzymes, we probed here its direct chemical
interaction with reactive oxygen species. The antibiotic did
not react with superoxide or (•)NO radicals, but peroxynitrite
(PON) was scavenged in the range of ∼1 μm minocycline and
below. The interaction of pharmacologically relevant
minocycline concentrations with PON was corroborated in
several assay systems and significantly exceeded the efficacy
of other antibiotics. Minocycline was degraded during the
reaction with PON, and the resultant products lacked
antioxidant properties. The antioxidant activity of
minocycline extended to cellular systems, because it prevented
neuronal mitochondrial DNA damage and glutathione depletion.
Maintenance of neuronal viability under PON stress was shown
to be solely dependent on direct chemical scavenging by
minocycline. We chose α-synuclein (ASYN), known from
Parkinsonian pathology as a biologically relevant target in
chemical and cellular nitration reactions. Submicromolar
concentrations of minocycline prevented tyrosine nitration of
ASYN by PON. Mass spectrometric analysis revealed that
minocycline impeded nitrations more effectively than
methionine oxidations and dimerizations of ASYN, which are
secondary reactions under PON stress. Thus, PON scavenging at
low concentrations is a novel feature of minocycline and may
help to explain its pharmacological activity.
PMID: 21081502 [PubMed] PMCID: PMC3037611
http://www.ncbi.nlm.nih.gov/pubmed/21081502
Full Text: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3037611/
Prevention of peroxynitrite-dependent tyrosine nitration and
inactivation of alpha1-antiproteinase by antibiotics.
Whiteman M, Halliwell B.
Free Radic Res. 1997 Jan;26(1):49-56.
Source: Neurodegenerative Disease Research Centre, King's College
London, UK.
Abstract
Peroxynitrite, formed by reaction of superoxide and nitric oxide,
appears to be an important tissue damaging species generated at
sites of inflammation. In this paper, we compare the abilities of
several antibiotics to protect against peroxynitrite-dependent
inactivation of alpha1-antiproteinase, and to inhibit tyrosine
nitration by peroxynitrite, in vitro. Tetracycline, minocycline,
doxycycline, rifamycin and rifampicin were highly protective in
both assay systems, whereas several other antibiotics tested were
not. The possibility that antibiotics could affect tissue injury
at sites of inflammation by scavenging peroxynitrite is discussed.
PMID: 9018471 [PubMed]
http://www.ncbi.nlm.nih.gov/pubmed/9018471
http://ukpmc.ac.uk/abstract/MED/9018471
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Updated: July
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