Re: juxtaposed

[Guest guest]

All,

And on a nanomolar basis, in in vitro experiments,

Thimerosal has been shown to be greater than

10 times more toxic than mercuric chloride

(HgCl2) to developing neuronal and fetal cells.

See: Geier DA, King PG, Geier MR. Mitochondrial

dysfunction, impaired oxidative-reduction

activity, degeneration, and death in human

neuronal and fetal cells induced by low-level

exposure to thimerosal and other metal compounds.

Toxicological & Environmental Chemistry 2009

June 4;91(4): 735 - 749.

Abstract

Thimerosal (ethylmercurithiosalicylic acid), an

ethylmercury (EtHg)-releasing compound (49.55%

mercury (Hg)), was used in a range of medical

products for more than 70 years. Of particular

recent concern, routine administering of Thimerosal-

containing biologics/childhood vaccines have become

significant sources of Hg exposure for some

fetuses/infants. This study was undertaken to

investigate cellular damage among in vitro human

neuronal (SH-SY-5Y neuroblastoma and 1321N1

astrocytoma) and fetal (nontransformed) model

systems using cell vitality assays and microscope-

based digital image capture techniques to assess

potential damage induced by Thimerosal and other

metal compounds (aluminum (Al) sulfate, lead (Pb)

(II) acetate, methylmercury (MeHg) hydroxide, and

mercury (Hg)(II) chloride) where the cation was

reported to exert adverse effects on developing

cells. Thimerosal-associated cellular damage was

also evaluated for similarity to pathophysiological

findings observed in patients diagnosed with

autistic disorders (ADs). Thimerosal-induced

cellular damage as evidenced by concentration- and

time-dependent mitochondrial damage, reduced

oxidative-reduction activity, cellular degeneration,

and cell death in the in vitro human neuronal and

fetal model systems studied. Thimerosal at low

nanomolar (nM) concentrations induced significant

cellular toxicity in human neuronal and fetal cells.

Thimerosal-induced cytoxicity is similar to that

observed in AD pathophysiologic studies. Thimerosal

was found to be significantly more toxic than the

other metal compounds examined. Future studies need

to be conducted to evaluate additional mechanisms

underlying Thimerosal-induced cellular damage and

assess potential co-exposures to other compounds

that may increase or decrease Thimerosal-mediated

toxicity.

Keywords: autism; glial; lead; mercury; mercuric;

neurodevelopmental

Hopefully, the newer article will help all to put

the information on the toxicity of inorganic mercury

(HgCl2) into prespective.

Respectfully,

G. King, PhD

http://www.dr-king.com

+++++++++++++++++++++++++++++++++++++++++++++++++++++

Quoting learningstillalways :

> Read this:

>

>

http://www.foodconsumer.org/newsite/Non-food/Drug/cerebrospinal_fluid_test_predi\

cts_alzheimer_s_disease_1008101135.html

>

> then these:

>

> J Neurochem. 2000 Jan;74(1):231-6.

> Mercury induces cell cytotoxicity and oxidative stress

> and increases beta-amyloid secretion and

> tau phosphorylation in SHSY5Y neuroblastoma cells.

> Olivieri G, Brack C, MŸller-Spahn F, StŠhelin HB,

> Herrmann M, Renard P, Brockhaus M, Hock C.

>

> Neurobiology Laboratory, Psychiatric University Hospital,

> Basel, Switzerland. Olivieri@...

> Abstract

> Concentrations of heavy metals, including mercury, have

> been shown to be altered in the brain and body fluids of

> Alzheimer's disease (AD) patients. To explore potential

> pathophysiological mechanisms we used an in vitro model

> system (SHSY5Y neuroblastoma cells) and investigated the

> effects of inorganic mercury (HgCl2) on oxidative stress,

> cell cytotoxicity, beta-amyloid production, and tau

> phosphorylation. We demonstrated that exposure of cells

> to 50 microg/L (180 nM) HgCl2 for 30 min induces a 30%

> reduction in cellular glutathione (GSH) levels (n = 13,

> p<0.001). Preincubation of cells for 30 min with 1 microM

> melatonin or premixing melatonin and HgCl2 appeared to

> protect cells from the mercury-induced GSH loss. Similarly,

> 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide

> (MTT) cytotoxicity assays revealed that 50 microg/L HgCl2

> for 24 h produced a 50% inhibition of MTT reduction (n = 9,

> p<0.001). Again, melatonin preincubation protected cells

> from the deleterious effects of mercury, resulting in MTT

> reduction equaling control levels. The release of beta-

> amyloid peptide (Abeta) 1-40 and 1-42 into cell culture

> supernatants after exposure to HgCl2 was shown to be

> different: Abeta 1-40 showed maximal (15.3 ng/ml) release

> after 4 h, whereas Abeta 1-42 showed maximal (9.3 ng/ml)

> release after 6 h of exposure to mercury compared with

> untreated controls (n = 9, p<0.001). Preincubation of cells

> with melatonin resulted in an attenuation of Abeta 1-40 and

> Abeta 1-42 release. Tau phosphorylation was significantly

> increased in the presence of mercury (n = 9, p<0.001),

> whereas melatonin preincubation reduced the phosphorylation

> to control values. These results indicate that mercury may

> play a role in pathophysiological mechanisms of AD.

>

> PMID: 10617124 [PubMed - indexed for MEDLINE]

>

> Rev Environ Health. 2006 Apr-Jun;21(2):105-17.

> Involvement of environmental mercury and lead in the

> etiology of neurodegenerative diseases.

> Monnet-Tschudi F, Zurich MG, Boschat C, Corbaz A, Honegger P.

>

> Department of Physiology, University of Lausanne, Switzerland.

> Florianne. Tschudi-Monnet@...

> Abstract

> The incidence of neurodegenerative disease like Parkinson's

> disease and Alzheimer's disease (AD) increases dramatically

> with age; only a small percentage is directly related to

> familial forms. The etiology of the most abundant, sporadic

> forms is complex and multifactorial, involving both genetic

> and environmental factors. Several environmental pollutants

> have been associated with neurodegenerative disorders. The

> present article focuses on results obtained in experimental

> neurotoxicology studies that indicate a potential pathogenic

> role of lead and mercury in the development of neuro-

> degenerative diseases. Both heavy metals have been shown to

> interfere with a multitude of intracellular targets, thereby

> contributing to several pathogenic processes typical of

> neurodegenerative disorders, including mitochondrial

> dysfunction, oxidative stress, deregulation of protein

> turnover, and brain inflammation. Exposure to heavy metals

> early in development can precondition the brain for developing

> a neurodegenerative disease later in life. Alternatively,

> heavy metals can exert their adverse effects through acute

> neurotoxicity or through slow accumulation during prolonged

> periods of life. The pro-oxidant effects of heavy metals can

> exacerbate the age-related increase in oxidative stress that

> is related to the decline of the antioxidant defense systems.

> Brain inflammatory reactions also generate oxidative stress.

> Chronic inflammation can contribute to the formation of the

> senile plaques that are typical for AD. In accord with this

> view, nonsteroidal anti-inflammatory drugs and antioxidants

> suppress early pathogenic processes leading to Alzheimer's

> disease, thus decreasing the risk of developing the disease.

> The effects of lead and mercury were also tested in

> aggregating brain-cell cultures of fetal rat telencephalon,

> a three-dimensional brain-cell culture system. The continuous

> application for 10 to 50 days of non-cytotoxic concentrations

> of heavy metals resulted in their accumulation in brain cells

> and the occurrence of delayed toxic effects. When applied at

> non-toxic concentrations, methylmercury, the most common

> environmental form of mercury, becomes neurotoxic under

> pro-oxidant conditions. Furthermore, lead and mercury induce

> glial cell reactivity, a hallmark of brain inflammation. Both

> mercury and lead increase the expression of the amyloid

> precursor protein; mercury also stimulates the formation of

> insoluble beta-amyloid, which plays a crucial role in the

> pathogenesis of AD and causes oxidative stress and

> neurotoxicity in vitro. Taken together, a considerable body

> of evidence suggests that the heavy metals lead and mercury

> contribute to the etiology of neurodegenerative diseases and

> emphasizes the importance of taking preventive measures in

> this regard.

>

> PMID: 16898674 [PubMed - indexed for MEDLINE]

>

> The future does not look bright.

>

>

>

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