CWD - Low Copper or High Manganese the Cause??
09-06-2002, 01:55 PM
#1
Thread Starter
Join Date: Feb 2003
Location: SE WI USA
Posts: 28
CWD - Low Copper or High Manganese the Cause??
http://www.purdeyenvironment.com/2MedHyp278.htm
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
Does a foreign cation substitution at prion protein's Cu domain initiate TSE?
M. Purdey Taunton, UK
Summary: .... Analyses of food chains supporting isolated clusters of sporadic TSEs (CWD in N Colorado, scrapie in Iceland, CJD in Slovakia) demonstrate a consistent 2 1/2 + fold greater concentration of the pro-oxidant divalent cation, manganese (Mn), in relation to normal levels recorded in adjoining TSE-free localities. Deficiencies of the antioxidant co factors Cu/Se/Zn/Fe and Mg, P and Na were also consistently recorded in TSE foodchains. Similarities between the clinical/pathological profile of TSEs and Mn delayed psycho-neurotoxicity in miners are cited, and a novel theory generated which suggests that sporadic TSE results from early life dependence of TSE susceptible genotypes on ecosystems characterised by this specific pattern of mineral imbalance. Low Cu/Fe induces an excessive absorption of Mn in ruminants and an increased oxidation of Mn2+ into its pro oxidant species, Mn3+, which accumulates in mitochondria of CNS astrocytes in Mn SOD deficient genotypes. Deficiencies of scavenger co factors Cu/Zn/Se/Fe in the CNS permits Mn3+ initiated chain reactions of auto-oxidant mediated neuronal degeneration to proliferate, which, in turn, up-regulates the expression of the Cu-metalloprotein, prion protein (PrP). Once the rate of PrP turnover and its demand for Cu exceeds the already depleted supply of Cu within the CNS, PrP can no longer bind sufficient Cu to maintain its conformation. Mn3+ substitutes at the vacated Cu domain on PrP thus priming up a latent capacity for lethal auto-oxidative activity to be carried along with PrP like a 'trojan horse'; where Mn3+ serves as the integral 'infectious' transmissible component of the misfolded PrP -cation complex. The Mn overactivation of concanavalin A binding to glycoprotein and Mn-initiated autoxidation results in a diverse pathological profile involving receptor capping, aggregation/modification of CNS membrane/cytoskeletal proteins. TSE ensues. The BSE/nv CJD strain entails a 'synthetic' induction of the same CNS mineral disturbance, where 'in utero' exposure to Cu-chelating insecticides/Mn supplements accelerates the onset of a more virulent 'strain' of adolescent TSE. © 2000 Harcourt Publishers Ltd
Edited by - Sag...again on 09/06/2002 15:01:24
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
Does a foreign cation substitution at prion protein's Cu domain initiate TSE?
M. Purdey Taunton, UK
Summary: .... Analyses of food chains supporting isolated clusters of sporadic TSEs (CWD in N Colorado, scrapie in Iceland, CJD in Slovakia) demonstrate a consistent 2 1/2 + fold greater concentration of the pro-oxidant divalent cation, manganese (Mn), in relation to normal levels recorded in adjoining TSE-free localities. Deficiencies of the antioxidant co factors Cu/Se/Zn/Fe and Mg, P and Na were also consistently recorded in TSE foodchains. Similarities between the clinical/pathological profile of TSEs and Mn delayed psycho-neurotoxicity in miners are cited, and a novel theory generated which suggests that sporadic TSE results from early life dependence of TSE susceptible genotypes on ecosystems characterised by this specific pattern of mineral imbalance. Low Cu/Fe induces an excessive absorption of Mn in ruminants and an increased oxidation of Mn2+ into its pro oxidant species, Mn3+, which accumulates in mitochondria of CNS astrocytes in Mn SOD deficient genotypes. Deficiencies of scavenger co factors Cu/Zn/Se/Fe in the CNS permits Mn3+ initiated chain reactions of auto-oxidant mediated neuronal degeneration to proliferate, which, in turn, up-regulates the expression of the Cu-metalloprotein, prion protein (PrP). Once the rate of PrP turnover and its demand for Cu exceeds the already depleted supply of Cu within the CNS, PrP can no longer bind sufficient Cu to maintain its conformation. Mn3+ substitutes at the vacated Cu domain on PrP thus priming up a latent capacity for lethal auto-oxidative activity to be carried along with PrP like a 'trojan horse'; where Mn3+ serves as the integral 'infectious' transmissible component of the misfolded PrP -cation complex. The Mn overactivation of concanavalin A binding to glycoprotein and Mn-initiated autoxidation results in a diverse pathological profile involving receptor capping, aggregation/modification of CNS membrane/cytoskeletal proteins. TSE ensues. The BSE/nv CJD strain entails a 'synthetic' induction of the same CNS mineral disturbance, where 'in utero' exposure to Cu-chelating insecticides/Mn supplements accelerates the onset of a more virulent 'strain' of adolescent TSE. © 2000 Harcourt Publishers Ltd
Edited by - Sag...again on 09/06/2002 15:01:24
09-06-2002, 02:05 PM
#2
Thread Starter
Join Date: Feb 2003
Location: SE WI USA
Posts: 28
RE: CWD - Low Copper or High Manganese the Cause??
Soil acidity has a direct effect upon availability of most essential plant nutrients. The best pH range for most nutrients is between 6.0 and 7.0. Deficiencies can be observed at both low and high pH's. Manganese and iron exhibit toxicity at low pH's and deficiency at high pH levels.
Micronutrients are required by plants in small amounts. Those essential for plant growth are boron (B), chloride (Cl), copper (Cu), iron (Fe), manganese (Mn), molybdenum (Mo) and zinc (Zn).
Most soils in Michigan, Indiana and Ohio contain adequate quantities of micronutrients. Field crop deficiencies of Cl, Mo and Fe have not been observed in this region of the United States. Some soils, however, may be deficient in B, Cu, Mn and Zn, and deficiencies can cause plant abnormalities, reduced growth and even yield loss. When called for, micronutrient fertilizers should be used judiciously and with care. Some micronutrient fertilizers can be toxic if added to sensitive crops or applied in excessive amounts.
Broadcast applications of Mn, however, are not recommended because of high soil fixation. Residual carryover of available Mn in deficient soils is very limited. Therefore, Mn fertilizers should be applied every year on these soils. Foliar-applied micronutrients are more frequently used when deficiency symptoms are present or suspected and when banded soil applications are not practical.
The three main classes of micronutrient sources are inorganic, synthetic chelates and natural organic complexes. Inorganic sources consist of oxides, carbonates and metallic salts such as sulfates, chlorides and nitrates. Sulfates of Cu, Mn and Zn are the most common metallic salts used in the fertilizer industry because of their high water solubility and plant availability.
Chelated Mn reactions in soil are quite different from chelated Zn reactions. Manganese chelates, when applied to soil, are usually ineffective because of high levels of available Fe in our soils (Fe replaces the Mn in soil-applied Mn chelates). Therefore, they are unacceptable sources of Mn when soil applied.
Common sources for Manganese (Mn)...
Manganese sulfate (23 to 25% Mn)
Manganese oxysulfates (variable % Mn)
http://www.agry.purdue.edu/ext/forag...RY%20NUTRIENTS
Edited by - Sag...again on 09/06/2002 15:09:07
Micronutrients are required by plants in small amounts. Those essential for plant growth are boron (B), chloride (Cl), copper (Cu), iron (Fe), manganese (Mn), molybdenum (Mo) and zinc (Zn).
Most soils in Michigan, Indiana and Ohio contain adequate quantities of micronutrients. Field crop deficiencies of Cl, Mo and Fe have not been observed in this region of the United States. Some soils, however, may be deficient in B, Cu, Mn and Zn, and deficiencies can cause plant abnormalities, reduced growth and even yield loss. When called for, micronutrient fertilizers should be used judiciously and with care. Some micronutrient fertilizers can be toxic if added to sensitive crops or applied in excessive amounts.
Broadcast applications of Mn, however, are not recommended because of high soil fixation. Residual carryover of available Mn in deficient soils is very limited. Therefore, Mn fertilizers should be applied every year on these soils. Foliar-applied micronutrients are more frequently used when deficiency symptoms are present or suspected and when banded soil applications are not practical.
The three main classes of micronutrient sources are inorganic, synthetic chelates and natural organic complexes. Inorganic sources consist of oxides, carbonates and metallic salts such as sulfates, chlorides and nitrates. Sulfates of Cu, Mn and Zn are the most common metallic salts used in the fertilizer industry because of their high water solubility and plant availability.
Chelated Mn reactions in soil are quite different from chelated Zn reactions. Manganese chelates, when applied to soil, are usually ineffective because of high levels of available Fe in our soils (Fe replaces the Mn in soil-applied Mn chelates). Therefore, they are unacceptable sources of Mn when soil applied.
Common sources for Manganese (Mn)...
Manganese sulfate (23 to 25% Mn)
Manganese oxysulfates (variable % Mn)
http://www.agry.purdue.edu/ext/forag...RY%20NUTRIENTS
Edited by - Sag...again on 09/06/2002 15:09:07
09-07-2002, 08:02 AM
#4
Fork Horn
Join Date: Feb 2003
Location: SE Wisconsin
Posts: 448
RE: CWD - Low Copper or High Manganese the Cause??
Low amounts of Copper (Cu) and/or High ammounts of Manganese (Mn) could help proteins/prions to mutate, could help/cause, assist CWD spread.
??? Are deer Mineral blocks high in Manganese? When feeding deer corn, are they getting enough Copper from natural browse?
??? Are deer Mineral blocks high in Manganese? When feeding deer corn, are they getting enough Copper from natural browse?
