A mechanism of mercury's damage of DNA, related mutations, and production of oxidative and peroxynitrite damage

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This is a mechanism of mercury's effects on those with conditions like autism,

ADHD, ALS, Alzheimer's, Parkinson's, etc.

(snipped)

(note: some recommend nitrous oxide use contraindicated in those with mercury

exposure due to this effect with mercury)

(also: mercury is known to cause increased glutamate activity)

Mercury and increased glutamate activate free radical forming processes like

xanthine oxidase which produce oxygen radicals and oxidative neurological

damage(346,142,13). Nitric oxide related toxicty caused by peroxynitrite formed

by the reaction of NO with superoxide anions, which results in nitration of

tyrosine residues in neurofilaments and manganese Superoxide Dimustase(SOD) has

been found to cause inhibition of the mitochondrial respiratory chain,

inhibition of the glutamate transporter, and glutamate-induced neurotoxicity

involved in ALS(524,521). Lipoic acid and N-acetylcysteine(NAC) also increase

glutathione levels and protect against superoxide radical/peroxynitrite damage,

so thus have an additional neuroprotective effect(494a,521,524,572c,54,56).

Mercury also blocks the immune function of magnesium and zinc (198,427,43,38),

whose deficiencies are known to cause significant neurological effects(461,463).

The low Zn levels result in deficient CuZnSuperoxide dismustase (CuZnSOD), which

in turn leads to increased levels of superoxide due to toxic metal exposure.

This is in addition to mercury’s effect on metallothionein and copper

homeostasis as previously discussed(477). 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.home.earthlink.net/~berniew1/amalg6.html