re: Copper toxicity

[Guest guest]

(Much of my info on copper toxicity is related to amalgam exposures and

interrellated with mercury)    This is from one of the papers on my web site.

 Mercury inhibits sulfur ligands in MT and in the case of intestinal cell

membranes inactivates MT that normally bind cuprous ions(477), thus allowing

buildup of copper to toxic levels in many and malfunction of the Zn/Cu SOD

function.

 

 

The level of mercury and copper released from high copper amalgam is as much as

50 times that of low copper amalgams(191).    Studies have consistently found

modern high copper non gamma-two amalgams have a high negative current and much

greater release of mercury vapor than conventional silver amalgams and are more

cytotoxic (35,258,298,299). Clinics have found the increased toxicity and higher

exposures to be factors in increased incidence of chronic degenerative

diseases(35,etc).   While the non gamma-two amalgams were developed to be less

corrosive and less prone to marginal fractures than conventional silver

amalgams, they have been found to be unstable in a different mechanism when

subjected to wear/polishing/ chewing/ brushing: they form droplets of mercury on

the surface of the amalgams(182,297).   This has also been found to be a factor

in the much higher release of mercury vapor by the modern non gamma-two

amalgams.    Recent studies have concluded that because the high mercury

release levels of modern amalgams, mercury poisoning from amalgam fillings is

widespread throughout the populationâ€(95,199,238,258).   Numerous other

studies also support this finding(Section IV).

 

  Copper is an essential trace metal which plays a fundamental role in the

biochemistry of the nervous system(489,495,464).    Several chronic

neurological conditions involving copper metabolic disorders are well documented

like ’s Disease and Menkes Disease.   Mutations in the copper/zinc

enzyme superoxide dismustase(SOD) have been shown to be a major factor in the

motor neuron degeneration in conditions like familial ALS and similar effects on

Cu/Zn SOD to be a factor in other conditions such as autism, Alzheimer’s,

Parkinson’s, and non-familial ALS(489,495,464,111).   This condition can

result in zinc deficient SOD and oxidative damage involving   nitric oxide,

peroxynitrite, and lipid peroxidation(495,496,489,524), which have been found to

affect glutamate mediated excitability and apoptosis of nerve cells and effects

on mitochondria(495,496,524,119) These effects can be reduced by zinc

supplementation(464,495), as well as supplementation with antioxidants and

nitric oxide-suppressing agents and peroxynitrite scavengers such as Vit C, Vit

E , lipoic acid, Coenzyme Q10, carnosine, gingko biloba, N-acetylcysteine,

etc.(237,444,464,494,495,469,521,524,572). Some of the antioxidants were also

found to have protective effects through increasing catalase and SOD action,

while reducing lipid peroxidations(494a).   Ceruloplasmin in plasma can   be

similarly affected by copper metabolism disfunction, like SOD function, and is

often a factor in neurodegeneration(489).

 

References:   www.flcv.com/amalg6.html

The urine fractionated porphyrin test might be useful in some cases related to

copper toxicity.