melatonin as a chelator & connection of mercury,melatoni n,fibromyalgia & Alzheimer's ,diabetes,other neurologicalconditions, e tc..]

[Guest guest]

> >

> > ++++++ Mercury Poisoning from Dental Amalgam

> <AMALGAM@L...> ++++++

> >

> > The following abstracts show that melatonin does bind toxic

metals

> and

> > provides the mercury connection to the one just posted on

> the

> > relation of fibromyalgia and melatonin level. Both mercury and

> EMF have

> > been shown to affect melatonin levels which has huge affects on

> lots of

> > health conditions. I found hundreds of studies in Medline on

> melatonin's

> > effect of reducing toxic effects of oxidative damage, affecting

> sleep

> > cycles, reducing intracellular calcium levels in the brain which

> mercury

> > causes, and lots of things.

> > Bernie

> > TITLE: The interaction of melatonin and its precursors with

> aluminium,

> > cadmium, copper, iron, lead, and zinc: an adsorptive voltammetric

> study.

> > AUTHORS: Limson J; Nyokong T; Daya S

> > AUTHOR AFFILIATION: Department of Chemistry, University,

> > Grahamstown, South Africa.

> > SOURCE: J Pineal Res 1998 Jan;24(1):15-21

> > CITATION IDS: PMID: 9468114 UI: 98127628

> > ABSTRACT:

> > Melatonin, a pineal secretory product, and its precursors,

> tryptophan and

> > serotonin, were examined for their metal binding affinities for

> both

> > essential and toxic metals: aluminium, cadmium, copper, iron,

> lead, and

> > zinc. An electrochemical technique, adsorptive stripping

> voltammetry, showed

> > the varying abilities of melatonin and its precursors to bind the

> metals in

> > situ.

> > The results show that the following metal complexes were formed:

> > aluminium with melatonin, tryptophan, and serotonin; cadmium with

> > melatonin and tryptophan; copper with melatonin and serotonin;

> iron(III)

> > with melatonin and serotonin; lead with melatonin, tryptophan, and

> > serotonin; and zinc with melatonin and tryptophan. Iron(II)

showed

> the

> > formation of an in situ complex with tryptophan only. These

> studies suggest

> > a further role for melatonin in the reduction of free radical

> generation and

> > metal detoxification, and they may explain the accumulation of

> aluminium in

> > Alzheimer's disease.

> > %%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%

> >

> > %%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%

> > TITLE: Mercury induces cell cytotoxicity and oxidative stress

> and

> > increases beta-amyloid secretion and tau phosphorylation in SHSY5Y

> > neuroblastoma cells.

> > AUTHORS: Olivieri G; Brack C; Muller-Spahn F; Stahelin HB;

> Herrmann M;

> > Renard P; Brockhaus M; Hock C

> > AUTHOR AFFILIATION:

> > Neurobiology Laboratory, Psychiatric University Hospital, Basel,

> > Switzerland. Olivieri@u...

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

> > CITATION IDS: PMID: 10617124 UI: 20083414

> > 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 athophysiological

> > mechanisms of AD.

> > ****************************************************************

> >

> > Inhibitory effects of melatonin on free intracellular calcium in

> mouse

> > brain cells. AUTHORS: Zhang QZ; Zhang JT

> > AUTHOR AFFILIATION:

> > Second Department of Pharmacology, Chinese

> Academy of

> > Medical Sciences, Beijing, China. zjtian@p...

> > SOURCE: Chung Kuo Yao Li Hsueh Pao 1999 Mar;20(3):206-10

> > CITATION IDS: PMID: 10452093 UI: 99381400

> > ABSTRACT:

> > AIM: To study the effects of melatonin (Mel) on cortical

> intrasynaptosomal

> > calcium concentration in old mice and on [Ca2+]i elevation

> induced by

> > Bay-K-8644, KCl, and sodium l-glutamate in isolated brain cells

of

> neonatal

> > mouse, and to determine the antiaging mechanism of Mel. METHODS:

> [Ca2+]i was

> > measured in an RF-5000 recording spectrofluorophotometer by

> preloading the

> > synaptosomes or cells with Fura 2-AM. RESULTS: Long term of

> administrating

> > Mel inhibited the overload of [Ca2+]i in old mouse cerebral

> cortex. The

> > [Ca2+]i in both high (20 mg.L-1) and low dose (1 mg.L-1) of Mel

> groups was

> > reduced from (434 +/- 32)nmol. L-1 (the older control group) to

> (330 +/- 41)

> > and (313 +/- 56) nmol.L-1, respectively, P < 0.01. Mel 0.01, 0.1,

> 1, and 3

> > mumol.L-1 remarkably reduced [Ca2+]i elevations in isolated

> newborn mouse

> > brain cells induced by Bay-K-8644, KCl, and Glu. CONCLUSIONS: The

> inhibitory

> > effect of Mel on neuronal [Ca2+]i overload is involved in its

> antiaging

> > effect.

> > %%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%

> >

> > +++++++++++++ http://www.listserv.gmd.de/archives/amalgam.html

> ++++++++++++++

> forwarded by Carol W.

--- End forwarded message ---

--- End forwarded message ---