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More Evidence supporting Purdey, Brown - free radical damage

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Kathy

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Low and behold, another confirmation of manganese and other metals capable of replacing copper on the PrPC protein, and leading to spongiform encephalopathy. To bad these researchers only tested transitional metals.

The evidence is stacking up in Mark Purdey's favour. No doubt these researchers have referenced Dr. DR Brown's work (Bath Univ. UK). Damge from oxidative stress being the main culprit causing neurotoxic damage. Brown's newest paper is entitled:

Neurodegeneration and oxidative stress: prion disease results from loss of antioxidant defence. Folia Neuropathol. 2005;43(4):229-43.

Department of Biology and Biochemistry, University of Bath, Bath, BA2 7AY, e-mail: [email protected]

Prion diseases or transmissible spongiform encephalopathies (TSEs) are rare neurodegenerative disorders that can be acquired either by direct transmission, inherited through dominant mutations in the prion protein gene or via an unknown sporadic cause. This latter group constitutes the vast majority of cases. Like many neurodegenerative diseases the hallmarks of oxidative damage can be readily detected throughout the brain of the affected individual. However, unlike most other neurodegenerative diseases, prion diseases are connected with a dramatic loss of antioxidant defence. As abnormal protein accumulates in the diseased brain there is both an increase of oxidative substances and a loss of the defences that keep them in check. In particular the normal cellular prion protein has been shown to be an antioxidant. Conversion of this protein to the protease resistant isoform is accompanied by a loss of this antioxidant activity. This change creates a paradox as the loss of activity is not accompanied by a loss of protein expression. It is likely that this prevents other cellular defences from responding sufficiently to protect neurons from the heightened oxidative burden. Recent experiments with transgenic mice have shown that when prion protein expression is switched off during the course of prion disease, cell death is dramatically halted and the mouse recovers from the disease. This result clearly illustrates that the continued expression of non-function prion protein is essential for disease progression. This implies that the presence of this abnormal protein during prion disease causes a failure of cellular antioxidant defence. This failed defence is the fundamental cause of the massive neurodegeneration that results in the fatal nature of TSEs. The role of oxidative stress in TSEs and other neurodegenerative disorders are discussed in this review.

PMID: 16416388


New support out of France.

Neurotoxicology. 2006 Feb 13; [Epub ahead of print]

Free radical generation of protease-resistant prion after substitution of manganese for copper in bovine brain homogenate.

Deloncle R, Guillard O, Bind JL, Delaval J, Fleury N, Mauco G, Lesage G.

Universite Francois Rabelais de Tours, Bio-Inorganic Chemistry Laboratory, Faculty of Pharmacy, 31 Avenue Monge, 37200 Tours, France.

The exchange between copper and seven transition metals is studied in a bovine brain obex homogenate according to the redox status of the medium. In reductive conditions, almost all the studied metals can substitute for copper when it is in the reduced form Cu(+). This substitution is reversible, since copper uptake as Cu(++) is restored in an oxidizing medium but only Co(++), Ni(++) and Mn(++), in this decreasing order, can substitute perfectly for copper in bovine brain homogenate. To study free radical effects on bovine brain proteins, at first a copper substitution was processed in order to inhibit superoxide dismutase-like protective properties against free radicals in copper metalloproteins. Manganese was selected since a brain copper decrease correlated with a manganese increase is well-known in transmissible spongiform encephalopathies. Results for bovine brain homogenate, initially negative in the Western blot Prionics((R)) test, indicate that the substitution of manganese for copper in a reducing medium and exposure to UVA-induced free radicals produce proteinase K resistant prion. These findings suggest that an impairment in brain metal homeostasis leading to oxidative abnormalities may be involved in transmissible spongiform encephalopathies.

PMID: 16481041 [PubMed - as supplied by publisher]
 

flounder

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BSE TOXICITY LINK 'NOT'



http://www.bseinquiry.gov.uk/files/yb/1988/01/28001001.pdf



Purdey beating his toxic BSe drums


http://www.bseinquiry.gov.uk/files/yb/1988/01/08001001.pdf




a) As regards the involvement of organophosphates in the origin of BSE, no
new scientific
information providing evidence or supporting the hypothesis by valid data
became
available after the adoption of the last opinion of the SSC on this issue.
Consequently
there is no reason for modifying the existing opinions.
b) Regarding the possibility of OP poisoning, the European legislation for
registration of
plant protection products and veterinary medicines – addressed in the
enquiries – provide
the basis for safe use of registered compounds and their formulations.
Regarding the
alleged intoxication cases reported and OP exposure it must be concluded
that safety
measures may not have been strictly followed.
References
Brown, D.R., Qin, K., Herms, J.W., Madlung, A., Manson, J., Strome, R.,
Fraser, P.E., Kruck, T., von
Bohlen, A., Schulz- Schaeffer, W., Giese, A., Westaway, D. and Kretzschmar,
H. (1997) The Cellular
Prion Protein Binds Copper In Vivo, Nature, 390, 684-7.
Purdey, M. (2000) Ecosystems Supporting Clusters of Sporadic TSEs
Demonstrate Excesses of the Radical-
Generating Divalent Cation Manganese and Deficiencies of Antioxidant
Co-Factors Cu, Se, Fe, Zn Medical
Hypotheses, 54, 278-306.
Scientific Steering Committee, 1998. Opinion on possible links between BSE
and Organophosphates. Adopted
on 25-26 June 1998
Scientific Steering Committee, 2001. Opinion on Hypotheses on the origin and
transmission of BSE. Adopted
on 29-30 November 2001.

http://europa.eu.int/comm/food/fs/sc/ssc/out356_en.pdf


transmission studies do not lie, amplification and transmission!


1: J Infect Dis 1980 Aug;142(2):205-8


Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to
nonhuman primates.

Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.

Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of
sheep and goats were transmitted to squirrel monkeys (Saimiri
sciureus) that were exposed to the infectious agents only by their
nonforced consumption of known infectious tissues. The asymptomatic
incubation period in the one monkey exposed to the virus of kuru was
36 months; that in the two monkeys exposed to the virus of
Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and
that in the two monkeys exposed to the virus of scrapie was 25 and
32 months, respectively. Careful physical examination of the buccal
cavities of all of the monkeys failed to reveal signs or oral
lesions. One additional monkey similarly exposed to kuru has
remained asymptomatic during the 39 months that it has been under
observation.

PMID: 6997404

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ui
ds=6997404&dopt=Abstract


and for Gods sake, if someone is smearing this [email protected] all over there kids
heads for lice and did not come up with a TSE, i would say this is good case
study;


UK FARMER WITH BSE


1) None of our animals that contracted BSE were treated with OP's, even
in utero.
2) My kids were treated with OP's as infants to control head lice. This
seems to be endemic as infection waves in UK primary schools (and
possibly elsewhere).
3) One might argue if the continued use of british beef in the UK was
ethical, none the less it happened. We have a duty to learn from it, not
least a duty to learn on behalf of those people who died so horribly....


However, i have never dusputed the remote possibility that ;


Phosmet induces up-regulation of surface levels of the cellular prion
protein.
Neuroreport. 9(7):1391-1395, May 11, 1998.
Gordon, Irit 1; Abdulla, Elizabeth M. 1; Campbell, Iain C. 1; Whatley,
Stephen A. 1,2
Abstract:
CHRONIC (2 day) exposure of human neuroblastoma cells to the organophosphate
pesticide phosmet induced a marked concentration-dependent increase in the
levels of PrP present on the cell surface as assessed by biotin labelling
and immunoprecipitation. Levels of both phospholipase C (PIPLC)-releasable
and non-releasable forms of PrP were increased on the plasma membrane. These
increases appear to be due to post-transcriptional mechanisms, since PrP
mRNA levels as assessed by Northern blotting were unaffected by phosmet
treatment. These data raise the possibility that phosmet exposure could
increase the _susceptibility to the prion agent by altering the levels of
accessible PrP_.

(C) Lippincott-Raven Publishers.


http://www.neuroreport.com/pt/re/neuroreport/abstract.00001756-199805110-000
26.htm;jsessionid=D3XI1RSXL8uyd5FtR23dvWP1753t5Cv0lY8VXIid8eyvzvuM7qJ5!-4778
99252!-949856144!9001!-1index=1&database=ppvovft&results=1&count=10&searchid
=1&nav=search



WHAT some of the OPiest/Metalist dont understand (refuse to understand to
further there plight to squash the truth of the ruminant feeding spreads and
amplifies the TSE agent) is that no where in science literature does it show
that Phosmet or metals _CAUSE_ TSE, there is a big difference. TO distort,
confuse, lie about the true aspect of this theory into trying to make people
believe that Phosmet and or Metals _CAUSE_ TSE, only weakens the whole
aspect of the study. but there will always be those that cannot admit the
truth about the amplification and transmission of TSE, want to blame others,
and will continue this deceit. ...TSS
 

rkaiser

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WHAT some of the OPiest/Metalist dont understand (refuse to understand to
further there plight to squash the truth of the ruminant feeding spreads and
amplifies the TSE agent) is that no where in science literature does it show
that Phosmet or metals _CAUSE_ TSE, there is a big difference. TO distort,
confuse, lie about the true aspect of this theory into trying to make people
believe that Phosmet and or Metals _CAUSE_ TSE, only weakens the whole
aspect of the study. but there will always be those that cannot admit the
truth about the amplification and transmission of TSE, want to blame others,
and will continue this deceit. ...TSS

Good gracious Valentine - What a statement.
Weaken the aspect of the study? What study? The study of feed transmission of misfolded prions? That is not a study, it is the accepted theory. The only study now is the race for the test which is all about that moral of all ground --- money thing.

The few people that are staying away from your "study" :lol: :lol: and seeking truth should not bother you Terry. You have the world on your side sweetie.

What is it that you fear from folks that don't follow you Terry. Nothing is being held back. If those who believe in the feed transmission of misfolded prions are correct, as you believe, what harm could a few outsiders cause?

Why the fear Terry?
 

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