Quoted message said:Subject: Re: thimerosal-news.com
From: "Jeff" [email hidden]
Date: 1/10/2004 1:03 PM Pacific Standard Time
Message-id: <[email hidden]>
"john" <[email hidden]> wrote in message
"]news:[email hidden]...
Quoted message said:thimerosal-news.comthimerosal-news.comOpen ↗
Thimerosal news offers information on the correlation between brain damage and autism that may
result from the exposure to the organic compound form of mercury contained in Thimerosal.
Vaccines containing Thimerosal and current legal suits are also reviewed.
Lots of press releases and a way to find a lawyer, yet there is no evidence here that Thimersal
causes anything.
Wrong.
Furthermore has nothing whatsoever to do with *famous buzz word* fear-mongoring.
(too long to post, read it ALL)
64.41.99.118mer haley.htmOpen ↗
Affidavit Of Boyd E. Haley. Professor And Chair. Department Of Chemistry. University Of Kentucky
Thimerosal Containing Vaccines and Neurodevelopment Outcomes
FORWARD:
Thimerosal or merthiolate is a derivative of thiolsalicylate where ethylmercury is attached though
the sulfur. It is defined as a preservative or anti microbial in medical use. This anti microbial
action is dependent on thimerosal breaking down releasing ethyl mercury that can penetrate cell
membranes and bind to intracellular enzymes, inhibiting them, and causing cell death. Further, in
certain biological environments the ethyl mercury can further break down releasing mercury cation
(Hg2+). Hg2+ is also very reactive with enzymes and proteins inhibiting their biological functions
and causing cell injury or death. Both ethyl mercury and Hg2+ are very neuro toxic compounds.
However? ethyl mercury is more rapidly partitioned into the hydrophobic (fatty) tissues of the
central nervous system and is a more potent neuro toxin than Hg2+ based on this "partitioning
factor". It is this partitioning factor that makes organic mercurials such as dimethyl mercury so
neuro toxically lethal (this is the compound that caused the death of a Dartmouth University
chemistry professor after she was exposed to a drop or two on her gloved hand). The concern with
organic mercurials, such as thimerosal, is that such compounds can be perceived as "pro toxicants"
just as certain pharmaceuticals can be classified as "pro drugs". This means that the original
compound, e.g. thimerosal, is less reactive giving the compound time to partition into certain areas
of the body before it breaks down releasing the ethyl mercury and then further releasing Hg2+.
However, while attaching ethyl mercury to thiolsalicylate makes the ethyl mercury less reactive it
most likely allows increased partitioning into the central nervous system before the ethylmercury is
released and thereby, increases the neuro toxicity per unit ethyl mercury involved. Considerable
caution must be taken when stating what is the "toxic level" of mercury and any mercury containing
compound. Humans are not rats in a pristine cage where their environment can be controlled to ensure
that other toxicities and infections are not occurring. The level of mercury that would cause
toxicity in a healthy individual is much higher than what would be needed to cause a toxic effect in
an individual that is ill or under oxidative stress. This is because additional stresses lower the
amount of protective compounds that bind mercury and render it less harmful. If an individual is low
on these protective compounds, then less mercury or thimerosal would be needed to cause a clinical
effect. Below I will present my interpretation of our research and that from other laboratories that
focus on the potential toxicity of injected thimerosal in the vaccine mixture.
BIOCHEMICAL TOXICITY STUDIES:
In my laboratory we have recently done an evaluation of the potential in vitro toxicity of vaccines
containing thimerosal as a "preservative" versus those vaccines not containing thimerosal. In these
preliminary studies, vaccines with thimerosal added consistently demonstrated in vitro toxicity that
was markedly greater than the non thimerosal or low thimerosal containing vaccines. We also compared
the toxicity of the vaccine solutions with solutions of pure thimerosal and with solutions of
mercury chloride. Mercury is a known neurotoxin and its mechanism of neurotoxicity has been studied
in our laboratory for the past 10 years. To determine the relative toxicity we used two different
biological testing systems: (i) brain homogenates and (ii) a mixture of four purified mammalian
enzymes. In human brain homogenates we had earlier observed that mercuric ion rapidly inhibited
tubulin viability at low micromolar levels. mimicking the situation in Alzheimer's diseased brain,
but was less toxic to actin (see Figures 1 & 2). Both tubulin and actin are polymerizing proteins
that are actively involved in neurite growth cone activity. In contrast to mercuric ion, vaccines
containing thimerosal inhibited both tubulin and actin viability (see Figure 3). This would indicate
that thimerosal has the potential to be much more damaging to neurite development than equivalent
levels of mercuric ion. It is my hypothesis that thimerosal releases ethyl mercury which most
certainly interferes with neurite growth and neuronal development in infants through rapid
inhibition of several thiol sensitive enzymes/proteins including actin, tubulin and creatine kinase.
This supports the concept that thimerosal in biological solutions injected into the human body could
cause a number of systemic problems identified as disease states.
CELL CULTURE WORK ON THIMEROSAL
The toxicity results obtained in our biochemical toxitity studies were not at all unexpected since
thimerosal and other compounds containing a similar thiol organic mercury group are widely known to
be especially potent neurotoxic agents. Our biochemical toxicity results are very consistent with
the reported toxicity of thimerosal containing vaccines versus nonthimerosal containing vaccines as
observed in cell culture studies (Kravchenko et al., Evaluation of the Toxic Action of Prophylatic
and Therapeutic Preparations on Cell (cultures
111. The Detection of Toxic Properties in Medical Biological Preparations by the [Degree of Cell
Damage in the L132 Continuous Cell Line. Zh. Mikrobiological Epidemiol. Immunobiol. (3):87 92,
1983). The results of this research demonstrated the toxicity of thimerosal (merthiolate) by
showing cell damage of the 1 :10,000 concentration found in vaccines after dilution of this
mixture to I part per 128. The conclusion was that thimerosal use for medical and biological
preparation (i.e. vaccines) manufacturing is inadmissible, especially in pediatrics. Other
studies on cytotoxicity of thimerosal compared it to another mercury containing preservative
(phenylmercuric acetate) and thimerosal was 5 times more toxic with only a two minute exposure
to the cells. The LD50 for thimerosal was 2.2 micrograms/ml for a 24 hour exposure to human
conjunctival cells and the comment was made that "the longer the contact time of these
preservatives, the severer the damage to the ocular tissue".
In collaboration with another professor in our department we have now included toxicity studies
using human brain neurons in culture. Our initial studies have shown that thimerosal is quite
toxic to these neurons in culture. Further, studies using vaccines with and without thimerosal
present demonstrated that the presence of thimerosal greatly enhanced the toxicity. The neuron
toxicity studies mirror the results we observed in the enzyme toxicity studies mentioned above
with the thimerosal being more toxic than inorganic mercury. Further studies are underway at the
present time.
(top) CASE HISTORIES ON THE TOXICITY OF THIMEROSAL AND OTHER ETHYL MERCURY RELEASING COMPOUNDS:
A recent review covers much of the case history literature on the little that is known about
ethylmercury toxicity (L. Magos Review on the Toxicity of Ethylmercury Including it.s Presence as a
Preservative in Biological and Pharmaceutical Products, J. Applied Toxicology 21. 1 5, 2001). The
conclusions reached by the author of this review is that "ethylmercury may present a risk when blood
mercury concentrations approaches or exceeds 1.0 microgram per ml and severe intoxication occurs
when blood mercury concentration approaches or exceeds 2 micrograms per ml." In the context of the
literature reviewed the conclusions by Dr. Magos seems reasonable. However, this conclusion was
based primarily on ethylmercury and methylmercury exposures from occupational exposures, dietary
intake, externally applied tinctures along with vaccination data on adults. It should be noted that
in considering deceased patients the one infant had a blood mercury (from an externally applied
tincture) that was measured at 1.34 micrograms per ml, a young boy had a blood mercury of 5
micrograms per ml (from eating pork from a pig feed ethylmercury) and adults had 15 micrograms per
ml (from eating bread made with seed treated with a compound that generated ethylmercury). Without
the needed extensive data to make a conclusion, it appears as if the younger the patient the more
deadly or toxic the ethylmercury is at a lower concentration. This is further supported by the other
(Kostial, K., et al. Influence of Age on Metal Metabolism and Toxicity, Environmental Health
Perspectives, v25, 81 86, 1978) who state "results obtained in sucklings show a very high intestinal
absorption of all metals which is partly attributed to milk diet; a higher whole body retention,
higher blood levels and a much higher accumulation in the brain". Certainly, no conclusion of sate
levels of exposure to ethylmercury on infants could be made from the data reviewed by Dr. Magos.
The exposures reviewed were from different delivery modalities and there is a considerable
difference in the toxicity of many materials when oral intake is compared to injections via the
vaccine route. Total mercury in the blood stream does not distinguish between bound mercury (e.g.
that coupled with glutathione and being removed from the body) and unreacted mercury (that available
to cause further damage). Ratios of bound and free ethylmercury are likely to be different if
ethylmercury is eaten or inhaled versus injected, bypassing the protective systems available in the
intestines. It was also pointed out in the review that the blood/urine ratios varied from 3.4 to 18
indicating that urine mercury levels are inferior for monitoring ethylmercury exposures. However,
since ethylmercury should partition between blood and urine at a consistent ratio this data could
also be interpreted to indicate that the mercury in some of these patients is coming from more than
just ethylmercury (e.g. dental amalgams that are the major source of human mercury body burden). In
a report on mercury levels in squirrel monkeys treated intranasally with thimerosal (Blair, A.,
Clark, B., Clarke, A and Wood, P., Tissue Concentrations of f Mercury After Chronic Dosing of
Squirrel Monkeys with Thimerosal Toxicology, v3, 171176, 1975) it was shown that exposure to 0.002%
thimerosal daily for 6 months, with a total of 2,280 ,ug given, lead to a 174/29 or about 6.0 ratio
of mercury in the brain/blood ratio indicating that thimerosal leads to a more rapid build up of
brain versus blood mercury. However, it was pointed out that the highest brain total (250ng/g) was
still below the 3 9 ug/g where neurological symptoms appear, but this later value would depend on
the oxidative stress of the patient and could be much lower.
The review states that "ethylmercury in medicinal preparations declines with time" and gave examples
of 38%, 64% and 85% decreases in ethylmercury in plasma and immunoglobin G samples. This mercury did
not disappear and the loss of ethylmercury has to be due to ethylmercury reacting covalently with
the protein thiols in the medicinal preparations. In aged medicinal preparations, increased
ethylmercury reaction with protein thiols in the preparations would likely change the neurotoxity
effects of the resulting mercury complexes compared to pure ethylmercury. How this pre reacted
ethylmercury would contribute to blood levels of mercury appears unknown, but it is likely to be
quite different from pure ethylmercury. However, what is known is that ethylmercury retains its
severe toxicity after prolonged exposure in living animals. This is supported by a case mentioned in
the Magos review where ethylmercury obtained by "consumption of meat from a pig fed with ethyl
mercury" caused severe damage to adults and killed two young boys. It seems as if ethylmercury can
retain its severe toxicity after a period of incubation time in a living pig, butchering and storage
of meat, followed by cooking. Then the concept that the faster decomposition of ethylmercury,
relative to methylmercury, decreases its toxicity compared to methylmercury seems to be such a small
difference as to be insignificant. What is solidly observed is that ethylmercury (and other organic
mercurials) can withstand considerable exposure to a living system, storage in a biological
environment, exposure to high heat in the presence of muscle tissue, and still produce a lethal
toxicity when taken orally.
In a 1972 a (National Geographic Quicksilver and Slow Death, vl 42, #4, 507527,
112) a similar report was presented where the pig was fed seed coated with Panogen, a methylmercury
pesticide. The family ate the pig as above and the four children suffered severe neurological
damage. But, in contrast to the ethylmercury poisoning above, they all lived. One of the
children was in utero during the consumption of the pork, suffered the most and was born blind
and mentally retarded. Again, this supports the concept that the younger the human the more
detrimental the toxic effect the organic mercury compounds will have.
It appears certain that much of the blood level mercury in these patients presented in the Magos
review could be from sources other than pure ethylmercury. In my opinion, I do not believe that a
safe level of ethylmercury can be arrived at by only comparing blood levels of mercury if we do not
know the chemical nature of all of the contributing mercury sources, the initial source of the
mercury or if the presence of other compounds were involved (e.g. antibiotics that bind heavy metals
such as tetracycline and enhance thimerosal toxicity:see below in Synergistic Toxicity).
It is of major concern that ethylmercury from thimerosal in vaccines is a special situation. It is
injected with millimolar levels of aluminum and it is probable that thimerosal, a negatively charged
molecule, has formed a salt compound with the positively charged aluminum cation that would change
its partitioning, breakdown rate, and may have a synergistic effect on the toxicity of any mercuric
ion produced from the ethylmercury. Aluminum is a known neurotoxin and to be causally involved in
macrophagic myofasciitis. The enhanced toxicity of ethylmercury in the presence of other toxic
agents is to be expected. Few of the clinical cases included in the Magos review were from vaccine
but the one that was discussed problems which occurred in a 44 year old adult with a blood mercury
of 0.104 ,ug per ml, so low that Dr. Magos called the diagnosis "unconvincing". Perhaps co
administration of thimerosal with aluminum in the Hepatitis B vaccine represents the "other
aetiological factors than ethylmercury" that might have been responsible for his mercury like
induced symptoms at such low concentrations. The authors of the report on this patient state "this
patient had evidence of previous environmental exposure to mercury" and this data can imply that
thimerosal is more toxic in patients previously exposed to materials that sensitize them.
(top)
DR. MAGOS REPORT TO THE IOM, SUMMER 2001:
DS. Magos makes several statements that reasonable individuals with scientific experience could
disagree about. First, "The consequence of faster decomposition is that, compared with
methylmercury. the neurotoxic potential of ethylmercury declines faster.?' This requires the
assumption that ethylmercury breaks down to Hg2+ as a toxic factor. What if the breakdown
product was a conjugate of cysteine known to enhance the toxicity of mercuric ion? What if the
breakdown was caused by reactive oxygen species generated in response to an infection? It is
known that ethylmercury breaks down 10 times faster in the presence of reactive oxygen species
(Suda, 1, and Takahashi, [l., Degradation of methyl and ethyl mercury into inorganic mercury by
other reactive oxygen species besides hydroxyl radical. Arch. Toxicol. 66, 34 39, 1992) making
the production of toxic Hg2+ occur more rapidly at sites of high level of reactive oxygen, and
in the body this would be at sites of infection or inflammation or within mitochondria, the
important energy producing organelle. In my opinion. the enhanced chemical ability to breakdown
ethylmercury versus methyl mercury at sites of reactive oxygen production (usually sites of
oxidative stress) makes ethylmercury a much more dangerous compound than methylmercury as it
attacks chemically at a site of infectious damage.
In section 2.b.a Dr. Magos quotes his research as showing that methylmercury treated rats had 1.55
(males) and 2.4 (females) the mercury in their brains as did ethylmercury treated rats. In addition,
the ethylmercury treated rats had
3.4 fold more inorganic mercury in their brains. He states that this "excludes the possibility
that the cleavage itself or the formed inorganic mercury is responsible for the brain damage. If
this were the case, the brain ethylmercury treated rats would be more affected than the brain of
methylmercury treated rats (which didn't occur by his analysis)." The problem with this
conclusion is that Dr. Magos expects the damage caused by methylmercury to be the same as that
caused by a combination of ethylmercury and 3.4 fold extra Hg2+. This is not likely as methyl
and ethyl mercury would partition into the hydrophobic areas of the brain whereas Hg2+ would
most likely react in the hydrophilic aspect of the brain. The inhibition of specific brain
enzymes by thimerosal (ethylmercury) compared to Hg2+ are markedly different.
SYNERGISTIC TOXICITY WITH THIMEROSAL:
Since about 1989 my laboratory has been actively involved in research regarding the toxic effects of
elemental mercury and the relationship of this toxicity to neurological diseases, primarily
Alzheimer's disease. One fact that has become extremely obvious to me during this past 11 years is
that it is impossible to determine the exact toxic level of mercury or mercury containing compounds
that is safe for all humans. There are several reasons why mercury should not be considered safe for
humans at the measurable levels currently reported as ' safe" by current government monitoring
agencies. One of these is the obvious effects of other metals on increasing the toxicity of
identical levels of mercury. An example is that of zinc ion, an essential metal for normal cell
function. Yet, in the presence of mercuric ion, the addition of zinc enhances the toxicity level
significantly (see Figure 4). Cadmium and lead are even more potent at enhancing the toxicity of
mercuric ion. This concept of synergistic toxicity of mercury with other metals is supported by
prior research that demonstrated that a mixture of mercury and lead at LD I levels of each metal
produced a mixture with an LD 100 effect, at least 50 times the additive effect minimally expected
(Schubert, J., Riley, E.J. and Tyler, S.A., Combined Effects in Toxicology-A Rapid Systematic
Testing Procedure: Cadmium, Mercury and Lead.
J. of Toxicology and Environmental Health, 4: 763 776, 19 8).
The synergistic effects of different compounds with thimerosal are not all known but some do exist.
For example, the commonly used antibiotic, tetracycline, is known to enhance thimerosal toxicity.
Crook and Freeman, Reactions Ind'~ced by the Concurrent Use of Thimerosal and Tetracycline, American
J. of Optometry & Physiological Optics v60,#9, pp759761 1983, reported that the use of tetracycline
in humans induced and increased the irritation and inflammation of the ocular tissues caused by
thimerosal. These results were confirmed in studies using rabbits. Therefore. it is obvious that
concurrent treatment of infants with other drugs and/or antibiotics has the possibility to enhance
the toxic effects of thimerosal exposures. Further, it was postulated that the synergistic effects
of tetracycline was due to the metal binding properties of this antibiotic that may have delivered
the toxic metal more effectively to the site(s) inducing enhanced toxicity. This data clearly
demonstrates that there is no know level of safety for the use of thimerosal, especially in infants
being treated with other medicinals that would enhance the toxicity of the ethyl mercury released
such as occurred with tetracycline (a commonly used antibiotic).
Since each human would likely have a level of toxicity from other mercury and non mercury containing
sources it would be impossible to determine the exact level of mercury that would induce observable
toxicity in each human. Many environmental toxicants could work synergistically with ethyl mercury
rendering the ethyl mercury much more toxic than it would be in the absence of these other toxicants
(e.g., elemental mercury from dental amalgams, cadmium from smoking, lead from paint and drinking
water, aluminum, etc.). Humans are not rats in a pristine cage, eating rat chow carefully prepared
to eliminate any toxicants. Humans smoke, drink alcohol, have numerous mercury emitting amalgam
fillings, eat questionable food, and drink water known to contain other toxicants. Finally, it is
impossible to state the toxic effect of any injection of thimerosal unless one knows the toxic
exposure of the individual to other heavy metals or other environmental toxicants.
(top) THE EFFECTS OF AGE AND HEALTH ON THIMEROSAL TOXITICY:
The detrimental effect of any specific level of mercury or mercury containing compound would have on
any one individual's metabolic system would be directly proportional to both the level of'
protective big compounds" (e.g., glutathione, metallothioine) that exist within that person on the
time of exposure and, the ability to physiologically clear such toxicants from the body. The level
of the protective compounds would certainly be directly dependent on two factors, age and health.
Infants, with their immature physiology and metabolism would not be expected to handle mercury as
efficiently as mature adults. The elderly have been shown to have decreased "protective" glutathione
levels compared to middle aged and young adults. Melatonin, a hormone, is known to be decreased in
the aged and melatonin is known to increase the neuron and cellular concentration of glutathione.
Glutathione is the natural compound that binds mercuric ion and aids in its removal from the body.
This explains partly why the aged are also more susceptible to oxidative toxicants such as mercury.
The elderly also have weakened immune systems and are more susceptible to microbial infections are
known to lower their chemical energy levels and, further, to reduce their ability to synthesize the
proteins that protect them from heavy metals. Infants have their own weaknesses regarding toxic
exposures. Infants do not make much bile in their early months of life and are less able to remove
mercury through bilary transport the major route for mercury removal. They also do not have a fully
developed renal system that would remove other heavy metals (e.g. aluminum! as effectively as
adults. The age factor must always be considered for response to heavy metal exposure as well as
spurious microbial infections.
THE EFFECTS OF GENETIC SUSCEPTIBILITY ON MERCURY TOXICITY:
Genetically susceptibility is of critical importance. For example, other researchers have shown that
genetic carriers of the brain protein APO E2 are protected against Alzheimer's disease (AD) whereas
genetic carriers of the APO E4 genotype are at enhanced risk factor for developing AD. APO E
proteins are synthesized in the brain with the assigned physiological task of carrying waste
material from the brain to the cerebrospinal fluid, across the blood brain barrier into the plasma
where the material is cleared by the liver. The biochemical difference between APO E2 and APO E4 is
that APO E2 has two additional thiol groups, capable of binding and removing mercury (and ethyl
mercury) that APO E4 does not have. The second highest concentration of APO E proteins is in the
cerebrospinal fluid. Therefore, it is my opinion that the protective effects of APO E2 is due to its
ability to protect the brain from exposure to oxidants like mercury and ethyl mercury by binding
these toxicants in the cerebrospinal fluid and keeping them from entering the brain. I strongly
object to labeling those "genetically susceptible" as "having a genetic disease" because they are
the first injured on exposure to modern toxicants. Humans did not evolve breathing mercury vapor or
having organicmercury compounds injected in them as infants.
SIMILARITY TO ACRODYNIA:
The argument that the thimerosal containing vaccines could not deliver the amount of mercury to
cause a systemic illness is somewhat refuted by the history of the disease classified as acrodynia.
Perhaps autism will end up like acrodynia, where the removal of the causative material (i.e. the
mercury containing teething powders) lead to cessation of the disease and the identification of the
cause. Due to the perceived low levels of mercury in the teething powders and the wide spread use of
mercury in medicine at that time it was 10 years after the removal of the mercury containing
teething powders before medicine acknowledged that mercury exposure was the causal factor. It is
significant to notice that many of the symptoms of acrodynia are similar to the clinical symptoms of
children identified today as autistic, with attention deficit disorder, etc. that have no family
history of such diseases or illness classifications.
SUMMARY:
It is the inability to see the effects of chronic, low level toxicities on human health that has
been, and remains, our greatest failing as intelligent beings. For example, within the past year two
publications in refereed scientific journals have emerged from major foreign research universities
demonstrating that mercury can induce the formation of three major pathological diagnostic hallmarks
of Alzheimer's disease. The production of these diagnostic hallmarks occurred at non lethal
concentrations near or below the levels of mercury reportedly found in most human brains. First,
mercury has been shown to induce an increase in amyloid protein secretion (the component of amyloid
plaques) and to increase the phosphorylation of a protein called Tau {see Oliveri et al., J. of
Neurochemistry, V 74, p231, 2000}, and to produce neurofibillary tangles {Leon" et al., NeuroReports
V12(4), 733, 2001 }. All of this was done with neurons in culture and represent observations found
and considered diagnostic of Alzheimer's disease. Further, in a very recent article by Dr. Ashley
Bush in the journal Neuron it is implied that Alzheimer's disease may be caused by heavy metal
buildup. This article focused on removal of zinc and copper by chelation decreasing amyloid plaque
formation in rats mercury was not studied. However, these metals, along with silver, are the
components of dental amalgams. This work is in agreement with data published earlier from my
laboratory in refereed articles and summarized in one single article {Pendergrass and Haley, Metal
Ions in Biological Systems V34, Chspter 16, Mercury and Its Effects on Environment and Biology,
Siegel and Sigel EDS., Marcel Dekker, Inc. I 996}. This data basically demonstrated that addition of
very low amounts of mercury to normal human brain homogenates inhibited critical thiol sensitive
enzymes (creatine kinase, glutamine synthetase and tubulin) that are also dramatically inhibited in
Alzheimer's diseased brain. Research in our laboratory clearly demonstrates that thimerosal rapidly
inhibits these enzymes as well as several other metabolically important enzymes.
Further, data presented in Aschner et al. in Methylmercury Alters Glutamate Transport in Astrocvtes
NeurochemistryInternational, v37, #2 3, pp 199 206, 2000 indicate that organic mercury compounds
dysregulate excitatory amino acid homeostasis and may cause glutamate mediated excitotoxic
mechanisms to be involved on exposures that cause neuron death or injury. Glutamate toxicity is one
hypothesis proposed to explain the slow deterioration of AD as it was reported that the enzyme,
glutamine synthetase, that removes toxic glutamate was elevated in AD cerebral spinal fluid (D.
Gunnersen and B. Haley, PNAS, USA, v89, 11949, 1992) and inhibited in AD brain (Butterfield et al.,
J. Neurochemistry, v68, 2451, 1997). Glutamine synthetase is rapidly inhibited by the divalent
mercuric ion as it has two divalent metal ion (manganese) binding sites required for activity. It is
obvious that ethyl mercury from thimerosal would have the same effect on glutamine synthetase as
mercury and methyl mercury and impair nervous system glutamate metabolism. Consistent with this
concept is the reported ability of astrocytes (the brain cells that contain glutamine synthetase
that converts toxic glutamate to non toxic glutamine) to preferentially concentrate brain organic
mercury (Ashner, Astrocytes as Modulators of Mercury lnduced Neurotoxicity Neurotoxicology vl 7, #3
4, pp663 669 1996).