Oh, Agent K......a thermometer dropped in a St. Paul School, and the
whole school was evacuated.

Why---according to the loop group Mercury is safe......http://kstp.com/
article/stories/S384578.shtml?cat=7

Dr. K--make sure you do not go to Sacramento, California's capital
city on
your vacation this summer-----they got a "C" grade when it came to
informing
the public about mercury in fish.

http://news.moneycentral.msn.com/provider/providerarticle.aspx?feed=ACBJ&date=20
080319&id=8364336

I hope you are able to tell who left town.  I certainly didn't leave.
Maybe it is time to tell your boss that she needs to lay off of you---
so you can
read the newsgroups with better eyes!

Doesn't matter.  The rule "you are what you eat" is
transitive.  I'm not being figurative, Sunshine.

And, yes, about that donkey?  Your a.s _is_ grass.

+---------- D. C. Sessions <dcs@lumbercartel.com> ----------+

So, you're saying that injecting something translates into 100%
absorption.
You're even dumber than we gave you credit for being and we extended
you more credit than the prime-plus housing market.

 "Methyl mercury is 95%-100% absorbed through the gut. It penetrates
 the blood brain barrier and the placenta. Elemental mercury vapors
 are 75%-85% absorbed. Elemental mercury is not well absorbed in the
 gut, but in the presence of yeast and unhealthy flora. It can be
 converted to methyl mercury and therefore absorbed. Inorganic
 mercury has 7-15% absorption through the gut and 2-3% absorption
 through the skin."

So much for your keen intuition, Cee.  You were only off by an order
of magnitude.

And then excreted, mostly via the feces.  A little detail that, like
so many others, escapes you.

 -- David Wright :: alphabeta at copper.net
    These are my opinions only, but they're almost always correct.
    "Without Bush, what will America's schoolchildren have to look down on?"
                                                       -- Bill Maher

On Mar 19, 7:03 pm, "Jan Drew" <jdrew1...@sbcglobal.net> wrote:

I went to Pubmed and found 299 articles on mitochondria and mercury.

All the articles were discussing inorganic mercury or methylmercury.

The various creatures studied were rats, Javan mongoose, dicentrarchus
labrax, the frog Rana Kl escolenta, porcine kidney and liver, zebra
fish, etc.

Since thimerosal has ethylmercury and no studies were done on human
tissue, am I correct in concluding that there is no valid scientific
data to implicate the mercury in thimerosal to human disease whether
inhaled, ingested, or injected?

DrCee
You cannot secure nor restore health with pus or poisons.

All you need to do is type *in humans*
You should know that!

http://www.ncbi.nlm.nih.gov/pubmed/17945343?ordinalpos=2&itool=EntrezSystem2.PEn
trez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

Histo-cytological responses of Dicentrarchus labrax (L.) following mercury
exposure.
Giari L, Simoni E, Manera M, Dezfuli BS.
Department of Biology and Evolution, University of Ferrara, Via Borsari, 46,
44100 Ferrara, Italy.

This work deals with the damaging effects of mercury (Hg concentrations 251,
355, 501mugl(-1)) on the structure and ultrastructure of gills, liver,
intestine and kidney of farmed European sea bass (Dicentrarchus labrax L.,
1758) acutely treated for 24 and 48h. The histoarchitecture of the gills of
exposed fish was highly modified due to severe oedema, telangiectasia and
secondary lamellar fusion. In hepatocytes and enterocytes hydropic cell
swelling, alterations to the endoplasmic reticulum and mitochondria were
noted, in addition to an abundance of myelinoid bodies which were frequently
encountered following treatment. In the intestine and renal tubules of
exposed European sea bass, rodlet cells (RCs) displayed ultrastructural
modifications. Statistical analyses were conducted on the number and the
size of selected cell types and structures. Following exposure to mercury
for 24 and 48h, the number of chloride cells, RCs and macrophage aggregates
were found to have increased significantly in the gills, the intestine and
the head kidney.

PMID: 17945343 [PubMed - as supplied by publisher]

http://www.ncbi.nlm.nih.gov/pubmed/17334523?ordinalpos=3&itool=EntrezSystem2.PEn
trez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

Involvement of glutamate and reactive oxygen species in methylmercury
neurotoxicity.
Aschner M, Syversen T, Souza DO, Rocha JB, Farina M.
Departments of Pediatrics and Pharmacology, Vanderbilt University Medical
Center, B3307 Medical Center North, Nashville, TN 37232, USA.
michael.aschner@vanderbilt.edu

This review addresses the mechanisms of methylmercury (MeHg)-induced
neurotoxicity, specifically examining the role of oxidative stress in
mediating neuronal damage. A number of critical findings point to a central
role for astrocytes in mediating MeHg-induced neurotoxicity as evidenced by
the following observations: a) MeHg preferentially accumulates in
astrocytes; b) MeHg specifically inhibits glutamate uptake in astrocytes; c)
neuronal dysfunction is secondary to disturbances in astrocytes. The
generation of reactive oxygen species (ROS) by MeHg has been observed in
various experimental paradigms. For example, MeHg enhances ROS formation
both in vivo (rodent cerebellum) and in vitro (isolated rat brain
synaptosomes), as well as in neuronal and mixed reaggregating cell cultures.
Antioxidants, including selenocompounds, can rescue astrocytes from
MeHg-induced cytotoxicity by reducing ROS formation. We emphasize that
oxidative stress plays a significant role in mediating MeHg-induced
neurotoxic damage with active involvement of the mitochondria in this
process. Furthermore, we provide a mechanistic overview on oxidative stress
induced by MeHg that is triggered by a series of molecular events such as
activation of various kinases, stress proteins and other immediate early
genes culminating in cell damage.

PMID: 17334523 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/17182013?ordinalpos=4&itool=EntrezSystem2.PEn
trez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

Brain Res. 2007 Feb 2;1131(1):1-10. Epub 2006 Dec 19.

Methylmercury induces oxidative injury, alterations in permeability and
glutamine transport in cultured astrocytes.
Yin Z, Milatovic D, Aschner JL, Syversen T, Rocha JB, Souza DO, Sidoryk M,
Albrecht J, Aschner M.
Department of Pediatrics, Vanderbilt University Medical Center, TN, USA.

The neurotoxicity of high levels of methylmercury (MeHg) is well established
both in humans and experimental animals. Astrocytes accumulate MeHg and play
a prominent role in mediating MeHg toxicity in the central nervous system
(CNS). Although the precise mechanisms of MeHg neurotoxicity are
ill-defined, oxidative stress and altered mitochondrial and cell membrane
permeability appear to be critical factors in its pathogenesis. The present
study examined the effects of MeHg treatment on oxidative injury,
mitochondrial inner membrane potential, glutamine uptake and expression of
glutamine transporters in primary astrocyte cultures. MeHg caused a
significant increase in F(2)-isoprostanes (F(2)-IsoPs), lipid peroxidation
biomarkers of oxidative damage, in astrocyte cultures treated with 5 or 10
microM MeHg for 1 or 6 h. Consistent with this observation, MeHg induced a
concentration-dependant reduction in the inner mitochondrial membrane
potential (DeltaPsi(m)), as assessed by the potentiometric dye,
tetramethylrhodamine ethyl ester (TMRE). Our results demonstrate that
DeltaPsi(m) is a very sensitive endpoint for MeHg toxicity, since
significant reductions were observed after only 1 h exposure to
concentrations of MeHg as low as 1 microM. MeHg pretreatment (1, 5 and 10
microM) for 30 min also inhibited the net uptake of glutamine
((3)H-glutamine) measured at 1 min and 5 min. Expression of the mRNA coding
the glutamine transporters, SNAT3/SN1 and ASCT2, was inhibited only at the
highest (10 microM) MeHg concentration, suggesting that the reduction in
glutamine uptake observed after 30 min treatment with lower concentrations
of MeHg (1 and 5 microM) was not due to inhibition of transcription. Taken
together, these studies demonstrate that MeHg exposure is associated with
increased mitochondrial membrane permeability, alterations in
glutamine/glutamate cycling, increased ROS formation and consequent
oxidative injury. Ultimately, MeHg initiates multiple additive or
synergistic disruptive mechanisms that lead to cellular dysfunction and cell
death.

PMID: 17182013 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/16918248?ordinalpos=7&itool=EntrezSystem2.PEn
trez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSumChem Res Toxicol. 2006 Aug;19(8):1080-5.Methylmercury induces pancreatic beta-cell apoptosis and dysfunction.Chen YW, Huang CF, Tsai KS, Yang RS, Yen CC, Yang CY, Lin-Shiau SY, Liu SH.Institute of Toxicology, Department of Laboratory Medicine, and Departmentof Orthopaedics, College of Medicine, National Taiwan University, Taipei,Taiwan.Mercury is a well-known toxic metal, which induces oxidative stress.Pancreatic beta-cells are vulnerable to oxidative stress. Thepathophysiological effect of mercury on the function of pancreaticbeta-cells remains unclear. The present study was designed to investigatethe effects of methylmercury (MeHg)-induced oxidative stress on the cellviability and function of pancreatic beta-cells. The number of viable cellswas reduced 24 h after MeHg treatment in a dose-dependent manner with arange from 1 to 20 microM. 2',7'-Dichlorofluorescein fluorescence as anindicator of reactive oxygen species (ROS) formation after exposure ofHIT-T15 cells or isolated mouse pancreatic islets to MeHg significantlyincreased ROS levels. MeHg could also suppress insulin secretion in HIT-T15cells and isolated mouse pancreatic islets. After 24 h of exposure to MeHg,HIT-T15 cells had a significant increase in mercury levels with adose-dependent manner. Moreover, MeHg displayed several features of cellapoptosis including an increase of the sub-G1 population and annexin-Vbinding. Treatment of HIT-T15 cells with MeHg resulted in disruption of themitochondrial membrane potential and release of cytochrome c from themitochondria to the cytosol and activation of caspase-3. AntioxidantN-acetylcysteine effectively reversed the MeHg-induced cellular responses.Altogether, our data clearly indicate that MeHg-induced oxidative stresscauses pancreatic beta-cell apoptosis and dysfunction.PMID: 16918248 [PubMed - indexed for MEDLINE]http://www.ncbi.nlm.nih.gov/pubmed/16764493?ordinalpos=9&itool=EntrezSystem2.PEn
trez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum1: J Prev Med Pub Health. 2006 May;39(3):199-204.[Mercuric chloride induces apoptosis in MDCK cells][Article in Korean]Lee JH, Youm JH, Kwon KS.Department of Preventive Medicine and Public Health, School of MedicineChonbuk National University.OBJECTIVES: Mercury is a hazardous organ-specific environmental contaminant.It exists in a wide variety of physical and chemical states, each of whichhas unique characteristics for the target organ specificity. Exposure tomercury vapor and to organic mercury compounds specifically affects the CNS,while the kidney is the target organ for inorganic Hg compounds. METHODS: Inthis study, mercury chloride (HgCl2) was studied in a renal derived cellsystem, i.e., the tubular epithelial Madin-Darby canine kidney (MDCK) cellline, which has specific sensitivity to the toxic effect of mercury. MDCKcells were cultured for 6-24 hr in vitro in various concentrations (0.1-100M) of HgCl2, and the markers of apoptosis or cell death were assayed,including DNA fragmentation, caspase-3 activity andwestern blotting ofcytochrome c. The influence of the metal on cell proliferation and viabilitywere evaluated by the conventional MTT test. RESULTS: The cell viability wasdecreased in a time and concentration dependent fashion: decreases werenoted at 6, 12 and 24 hr after HgCl2 exposure. The increases of DNAfragmentation were also observed in the concentrations from 0.1 to 10 M ofHgCl2 at 6 hr after exposure. However, we could not observe DNAfragmentation in the concentrations more than 25 M because the cells rapidlyproceeded to necrotic cell death. The activation of caspase-3 was alsoobserved at 6 hr exposure in the HgCl2 concentrations from 0.1 to 10 M. Therelease of cytochrome c from the mitochondria into the cytosol, which is aninitiator of the activation of the caspase cascade, was also observed in theHgCl2-treated MDCK cells. CONCLUSIONS: These results suggest that theactivation of caspase-3 was involved in HgCl2-induced apoptosis. The releaseof cytochrome c from the mitochondria into the cytosol was also observed inthe HgCl2-treated MDCK cells. These findings indicate that in MDCK cells,HgCl2 is a potent inducer of apoptosis via cytochrome c release from themitochondria.PMID: 16764493 [PubMed - indexed for MEDLINE]http://www.ncbi.nlm.nih.gov/pubmed/16457873?ordinalpos=11&itool=EntrezSystem2.PE
ntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum1: Sci Total Environ. 2006 Aug 1;366(2-3):627-37. Epub 2006 Feb 7Accumulation of mercury, selenium and their binding proteins in porcinekidney and liver from mercury-exposed areas with the investigation of theirredox responses.Chen C, Qu L, Zhao J, Liu S, Deng G, Li B, Zhang P, Chai Z.Key Laboratory of Nuclear Analytical Techniques and Institute of High EnergyPhysics, Chinese Academy of Sciences, P. O. Box 918, Beijing 100039, PRChina. chenchy@mail.ihep.ac.cnThe subcellular localization of Se and Hg and their cytosolic bindingproteins, including cellular oxidative status, in porcine liver and kidneyhave been studied by using samples from a chronic Hg-contaminated area and anon-Hg-contaminated area. Coaccumulation and redistribution of Se and Hg insubcellular fractions due to mercury exposure were found. The Hg and Seconcentrations in tissues from Hg-exposed porcine were 80 fold and 5-20 foldhigher than controls, respectively. Interestingly, the retention of both Seand Hg increased 10% in mitochondria, while decreased 10% in cytosol ofHg-exposed pig liver. Mercury was mainly in the form of MTs in the cytosolof the non-Hg-exposed porcine kidney. MT binds Hg in the cytosol withlimited capacity, and the rest Hg was redistributed to the high molecularweight (MW) proteins (80-100 kDa) in the Hg-exposed group. Thecoaccumulation of Hg and Se was also found in high MW proteins, where theirmolar ratio tended to be 1:1. Moreover, the Se-containing polypeptides (3-6kDa) increased significantly both in hepatic and renal cytosol of theHg-exposed pigs. Se-dependent GSH-Px and SOD activity were increased to copewith Hg-induced oxidative stress. In previous studies, the roles of Se andMTs were generally taken into account separately; we discussed theircombining roles in the case of high Hg exposure. The present results werebeneficial to understand the existing states of Hg in vivo and evaluate theinteraction of toxic and essential elements.PMID: 16457873 [PubMed - indexed for MEDLINE]http://www.ncbi.nlm.nih.gov/pubmed/17182013?ordinalpos=1&itool=EntrezSystem2.PEn
trez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum1: Brain Res. 2007 Feb 2;1131(1):1-10. Epub 2006 Dec 19.  LinksMethylmercury induces oxidative injury, alterations in permeability andglutamine transport in cultured astrocytes.Yin Z, Milatovic D, Aschner JL, Syversen T, Rocha JB, Souza DO, Sidoryk M,Albrecht J, Aschner M.Department of Pediatrics, Vanderbilt University Medical Center, TN, USA.The neurotoxicity of high levels of methylmercury (MeHg) is well establishedboth in humans and experimental animals. Astrocytes accumulate MeHg and playa prominent role in mediating MeHg toxicity in the central nervous system(CNS). Although the precise mechanisms of MeHg neurotoxicity areill-defined, oxidative stress and altered mitochondrial and cell membranepermeability appear to be critical factors in its pathogenesis. The presentstudy examined the effects of MeHg treatment on oxidative injury,mitochondrial inner membrane potential, glutamine uptake and expression ofglutamine transporters in primary astrocyte cultures. MeHg caused asignificant increase in F(2)-isoprostanes (F(2)-IsoPs), lipid peroxidationbiomarkers of oxidative damage, in astrocyte cultures treated with 5 or 10microM MeHg for 1 or 6 h. Consistent with this observation, MeHg induced aconcentration-dependant reduction in the inner mitochondrial membranepotential (DeltaPsi(m)), as assessed by the potentiometric dye,tetramethylrhodamine ethyl ester (TMRE). Our results demonstrate thatDeltaPsi(m) is a very sensitive endpoint for MeHg toxicity, sincesignificant reductions were observed after only 1 h exposure toconcentrations of MeHg as low as 1 microM. MeHg pretreatment (1, 5 and 10microM) for 30 min also inhibited the net uptake of glutamine((3)H-glutamine) measured at 1 min and 5 min. Expression of the mRNA codingthe glutamine transporters, SNAT3/SN1 and ASCT2, was inhibited only at thehighest (10 microM) MeHg concentration, suggesting that the reduction inglutamine uptake observed after 30 min treatment with lower concentrationsof MeHg (1 and 5 microM) was not due to inhibition of transcription. Takentogether, these studies demonstrate that MeHg exposure is associated withincreased mitochondrial membrane permeability, alterations inglutamine/glutamate cycling, increased ROS formation and consequentoxidative injury. Ultimately, MeHg initiates multiple additive orsynergistic disruptive mechanisms that lead to cellular dysfunction and celldeath.PMID: 17182013 [PubMed - indexed for MEDLINE]http://www.ncbi.nlm.nih.gov/pubmed/16366737?ordinalpos=2&itool=EntrezSystem2.PEn
trez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSumNeurodegeneration from mitochondrial insufficiency: nutrients, stem cells,growth factors, and prospects for brain rebuilding using integrativemanagement.Kidd PM.University of California, Berkeley, USA. dockidd@dockidd.comDegenerative brain disorders (neurodegeneration) can be frustrating for bothconventional and alternative practitioners. A more comprehensive,integrative approach is urgently needed. One emerging focus for interventionis brain energetics. Specifically, mitochondrial insufficiency contributesto the etiopathology of many such disorders. Electron leakages inherent tomitochondrial energetics generate reactive oxygen free radical species thatmay place the ultimate limit on lifespan. Exogenous toxins, such as mercuryand other environmental contaminants, exacerbate mitochondrial electronleakage, hastening their demise and that of their host cells. Studies of thebrain in Alzheimer's and other dementias, Down syndrome, stroke, Parkinson'sdisease, multiple sclerosis, amyotrophic lateral sclerosis, Huntington'sdisease, Friedreich's ataxia, aging, and constitutive disorders demonstrateimpairments of the mitochondrial citric acid cycle and oxidativephosphorylation (OXPHOS) enzymes. Imaging or metabolic assays frequentlyreveal energetic insufficiency and depleted energy reserve in brain tissuein situ. Orthomolecular nutrients involved in mitochondrial metabolismprovide clinical benefit. Among these are the essential minerals and the Bvitamin group; vitamins E and K; and the antioxidant and energetic cofactorsalpha-lipoic acid (ALA), ubiquinone (coenzyme Q10; CoQ10), and nicotinamideadenine dinucleotide, reduced (NADH). Recent advances in the area of stemcells and growth factors encourage optimism regarding brain regeneration.The trophic nutrients acetyl L-carnitine (ALCAR), glycerophosphocholine(GPC), and phosphatidylserine (PS) provide mitochondrial support andconserve growth factor receptors; all three improved cognition indouble-blind trials. The omega-3 fatty acid docosahexaenoic acid (DHA) isenzymatically combined with GPC and PS to form membrane phospholipids fornerve cell expansion. Practical recommendations are presented forintegrating these safe and well-tolerated orthomolecular nutrients into acomprehensive dietary supplementation program for brain vitality andproductive lifespan.PMID: 16366737 [PubMed - indexed for MEDLINE]