Tylenol depletes Glutathione (necessary for removal of mercury)

[Guest guest]

your liver is already taxed in illness and

working overtime. Add insult to injury by making

it detox tylenol which is so very hard on the liver

http://www.wellness.com/blogs/DrMarkham/51/what-every-user-of-acetaminophen\

-needs-to-know/dr-laura-markham

" The danger is that there isn't much difference

between a safe, effective dose, and a toxic dose.

Just a doubling of the maximum daily dose can be

enough to kill, warns Dr. Anne Larson of the

University of Washington Medical Center. The

other problem is that if you have no food in your

stomach, or if you have alcohol in your system,

or worse yet, both, (not relevant for your kids

unless they're teenagers, but think about that

tylenol you took for your hangover last month),

the regular dosage can be toxic because of the overload to the liver. "

COMMENT

" Glutathione is found in every one of the

trillions of cells in the body. It is most

abundant in the liver and then the kidneys. These

are the detoxifying organs. NAC N-acetyl cystiene

is provided to patients in every hospital

emergency situation in the USA for acetaminophen

overdose. However NAC has many side effects to

the health of the individual, but the alternative

is certain death. So it is only administered in emergency room situations. "

http://www.mercola.com/2005/may/17/tylenol_risk.htm

" Most experts believe Tylenol causes its damage

by depleting glutathione. If you keep your

glutathione levels up, the damage from the

Tylenol may be largely preventable. Even

conventional medicine recognizes this, as anyone

who overdoses on Tylenol receives large doses of NAC in the emergency room. "

http://www.sciencedaily.com/releases/2002/10/021014072451.htm

" An overdose of acetaminophen can cause depletion

of glutathione and land a person in the hospital.

" Acetaminophen toxicity is the number one cause

of hospital admission for liver failure in the United States, " he said. "

http://www.benbest.com/nutrceut/NAC.html

" Glutathione detoxifies acetaminophen, but once

glutathione is depleted there can be significant

cell death in the liver [THE AMERICAN JOURNAL OF

MEDICINE; Flanagan,RJ; 91(Suppl C):131S-139S

(1991)]. AIDS victims can suffer severe liver and

kidney damage by using acetaminophen or alcohol,

which severely deplete glutatione [PROCEEDINGS OF

THE NATIONAL ACADEMY OF SCIENCES (USA);

Herzenberg,LA; 94(5):1967-1972 (1997)]. "

http://www.ssafood.com/site/docsTopicsTips/Nourish%20Your%20Eyes.mht

" Glutathione, another antioxidant, also prevents

cataracts. In fact, lenses with cataracts contain

one-fifteenth (1/15th) of the normal amount of

glutathione and one-tenth (1/10th) the normal

level of vitamin C. Glutathione is in asparagus,

avocado, broccoli, garlic, onions, spinach,

tomatoes, watermelon, eggs and walnuts. Abel

advises taking alpha lipoic acid, N-acetyl

cysteine and selenium, which contribute to

glutathione production. Abel notes that

metabolizing and excreting acetaminophen

(Tylenol) depletes glutathione. “Tylenol is

probably not the best long-term pain reliever for

anyone concerned with eye health.” He says. "

GOOGLE ON +glutathione+tylenol

http://www.gotdownsyndrome.net/glutathione & acetaminophen.html

Glutathione & The Acetaminophen (active ingredient in Tylenol) Issue:

Glutathione is commonly deficient in individuals

with Down Syndrome, due to the extra chromosome &

overexpression of the SOD-1 gene. Glutathione is

an important antioxidant. It helps scavenge free

radicals, deal with oxidative stress & the

pro-oxidant state of individuals with Down

Syndrome. Acetaminophen (the active ingredient in

Tylenol & many other OTC drugs), depletes

Glutathione levels in the liver (where it is made

& stored). Therefore, for a person with Down

Syndrome, this situation is very important. Since

Acetaminophen depletes Glutathione (which is

already deficient in DS), it is a bad situation -

a key antioxidant is being even more depleted. It

can then cause more oxidative damage, free

radicals & liver damage. Tylenol is known to

possibly cause liver damage & failure. It is best

if Tylenol (and drugs containing Acetaminophen)

be avoided, but if it is necessary, they can be

used at times. When you have to use them, just

make sure you give more Glutathione or

N-acetyl-cysteine to help out! Below, is alot of

info on Glutathione & the Acetaminophen issue

(since it is an important issue that comes up fairly often on DS lists):

The following is a list of some of the drugs that contain Acetaminophen:

Actifed Plus

Anacin (all products)

Benadryl (Plus and Plus Nighttime)

Comtrex (all products)

Dristan (all products except Room Vaporizer)

Drixoral Plus

Excedrin (all products)

Nyquil Nighttime Cold Medicine

Pamprin (all products)

Panadol, Children's and Infant's

Percogesic

Sinutab (all products)

Sominex Pain Relief Formula 1 Tablets

TheraFlu (all products)

Tylenol (all products)

Paracetomal

from:

http://www.mdanderson.org/topics/paincontrol/display.cfm?id=34E2C00E-5D6A-44A1-8\

317170F0DAB8D54 & method=displayFull

This article is one of the best articles I have

seen on Glutathione. It talks about the numerous

things that Glutathione is involved with. It also

talks about Acetaminophen & Glutathione. The

article also does not talk with too many " big

words " & things that are really hard to

understand. http://www.thorne.com/altmedrev/fulltext/glut.html

Here are a couple quotes from the above article

about Acetaminophen (with a few notes of mine):

" Many pharmaceutical products are oxidants

capable of depleting GSH [my note: Glutathione]

from the liver, kidneys, heart, and other

tissues.29 The popular over-the-counter drug

acetaminophen [my note: active ingredient inÂ

Tylenol] is a potent oxidant [my note: it creates

oxidation - free radicals]. It depletes GSH from

the cells of the liver [my note: which is where

GSH is made & stored], and by so doing renders

the liver more vulnerable to toxic damage. "

" The consequences of sustained GSH depletion are

grim. As cellular GSH is depleted, first

individual cells die in those areas most affected

[my note: we have lots of cell death already

going on in DS]. Then zones of tissue damage

begin to appear; those tissues with the highest

content of polyunsaturated lipids and/or the most

meager antioxidant defenses are generally the

most vulnerable. Localized free-radical damage

[my note: which is an issue in DS, due to low

antioxidant levels & high oxidative stress]

spreads across the tissue in an ever-widening,

self-propagating wave. If this spreading wave of

tissue degeneration is to be halted, the

antioxidant defenses must be augmented. "

This is an interesting abstract that says that

Resveratrol helps against the toxicity done by

Acetaminophen. Resveratrol is a potent

antioxidant - it is from the skin of grapes. If

you have to give Tylenol, it sounds like it'd be

very beneficial to give Resveratrol also:

Protective effects of resveratrol against

acetaminophen-induced toxicity in mice.

Marmara University, School of Pharmacy,

Departments of Pharmacology, Istanbul, Turkey.

This investigation elucidates the role of free

radicals in acetaminophen (AA)-induced toxicity

and the possible protection by resveratrol (RVT).

BALB-c mice were injected with a single dose of

900mg/kg AA to induce toxicity, while RVT

administred in a dose of 30mg/kg i.p. following

AA. Mice were sacrificed 4h after AA injection to

determine serum ALT, AST and tumor necrosis

factor-alpha (TNF-alpha) levels in blood, and

glutathione (GSH), malondialdehyde (MDA) levels,

myeloperoxidase (MPO) activity and collagen

contents in liver tissues. Formation of reactive

oxygen species in hepatic tissue samples was

monitored by using chemiluminescence (CL)

technique with luminol and lucigenin probe. ALT,

AST levels and TNF-alpha were increased

significantly after AA treatment, and reduced

with RVT. AA caused a significant decrease in GSH

levels while MDA levels and MPO activity were

increased in liver tissues. On the other hand

when RVT administered following AA, depletion of

GSH and accumulation of MDA and neutrophil

infiltration were reversed back to control.

Furthermore increased luminol and lucigenin CL

levels in the AA group reduced by RVT treatment.

Our results implicate that AA causes oxidative

damage in hepatic tissues and RVT, by its potent

antioxidant effects protects the liver tissue.

These data suggest that RVT may be of therapeutic

use in preventing hepatic oxidative injury due to AA toxicity.

-----------------------

Someone asked for some articles/abstracts to take

to their doctor to show him the importance of

Glutathione in Down Syndrome & the issue of

Acetaminophen. So, I figured it'd be good to

compile a bunch of abstracts & articles that show

the Acetaminophen issue, the pro-oxidant state

already present in an individual with Down

Syndrome & their deficiency of Glutathione. Below is that info:

Abstracts showing elevated oxidative stress,

pro-oxidant state & glutathione deficiency in DS -

Multiple evidence for an early age pro-oxidant state in Down Syndrome patients.

Department of Physiology, University of Valencia, E-46010, Valencia, Spain.

Oxidative stress has been associated with Down

syndrome (DS) and with its major phenotypic

features, such as early ageing. In order to

evaluate an in vivo pro-oxidant state, the

following analytes were measured in a group of DS

patients aged 2 months to 57 years: (a) leukocyte

8-hydroxy-2'-deoxyguanosine (8-OHdG); ( blood

glutathione; © plasma levels of: glyoxal (Glx)

and methylglyoxal (MGlx); some antioxidants (uric

acid, UA, ascorbic acid, AA and Vitamin E), and

xanthine oxidase (XO) activity. A significant

1.5-fold increase in 8-OHdG levels was observed

in 28 DS patients vs. 63 controls, with a sharper

increase in DS patients aged up to 30 years. The

GSSG:GSHx100 ratio was significantly higher in

young DS patients (< 15 years), in contrast to DS

patients aged >/=15 years that showed a

significant decrease in the GSSG:GSHx100 ratio

ratio vs. controls of the respective age groups.

Plasma Glx levels were significantly higher in

young DS patients, whereas no significant

difference was detected in DS patients aged >/=15

years. Unlike Glx, the plasma levels of MGlx were

found to be significantly lower in DS patients

vs. controls. A significant increase was observed

in plasma levels of UA in DS patients that could

be related to an increased plasma XO activity in

DS patients. The plasma concentrations of AA were

also increased in young (< 15 years) DS patients,

but not in older patients vs. controls in the

same age range. The levels of Vitamin E in DS

patients did not differ from the values

determined in control donors. The evidence for a

multiple pro-oxidant state in young DS patients

supports the role of oxidative stress in DS

phenotype, with relevant distinctions according to patients' ages.

Glutathione metabolism and antioxidant enzymes in children with Down syndrome.

Laboratory of Biochemistry, Molecular Medicine

Unit, Children's Hospital and Research Institute Bambino Gesu, Rome, Italy.

Oxidative stress has been proposed as a

pathogenic mechanism of atherosclerosis, cell

aging, and neurologic disorders in Down syndrome.

This study demonstrates a systemic decrease of

all glutathione forms, including

glutathionyl-hemoglobin, in the blood of children

with Down syndrome. Furthermore, we obtained a

disequilibrium, in vivo, between the antioxidant enzyme activities.

Diminished glutathione levels cause spontaneous

and mitochondria-mediated cell death in neurons

from trisomy 16 mice: a model of Down's syndrome.

Institut fur Physiologie der Charite, Humboldt

Universitat Berlin, Germany. sebastian.schuchmann@...

It has been suggested that the increased neuronal

death in cultures from trisomy 16 (Ts16) mice, a

model of Down's syndrome, might result from a

diminished concentration of reduced glutathione

(GSH). In this study we used microfluorometric

techniques to investigate the effect of GSH

levels on neuronal survival in diploid and Ts16

cultures. Addition of the GSH precursors cysteine

and cystine and the antioxidant tocopherol to the

culture medium increased the GSH concentration up

to 126.0% in diploid and up to 111.9% in Ts16

neurons. Moreover, we observed a reduced

spontaneous neuronal death rate in diploid and

Ts16 cultures. Following the application of

50-100 microM glutamate to culture medium, we

found a GSH increase in the presence of cysteine,

cystine, tocopherol, and cyclosporin A, an

inhibitor of mitochondrial permeability

transition (diploid, 105.8-110.8%; Ts16,

83.1-96.3%). However, only tocopherol and

cyclosporin A had a protective effect on

glutamate-induced neuronal death. The results

suggest that reduced GSH levels affect the

increase of a spontaneous and a

mitochondria-mediated, cyclosporin A-sensitive

type of neuronal cell death. Therefore, elevating

intracellular GSH concentration may have

neuroprotective effects in Down's syndrome and Alzheimer's disease.

Glutathione levels and nerve cell loss in

hippocampal cultures from trisomy 16 mouse--a model of Down syndrome.

Department of Neurophysiology, Humboldt University, Berlin, Germany.

The tripeptide glutathione (reduced state, GSH)

is an important intracellular free radical

scavenger protecting cells against oxidative

stress. The trisomy 16 mouse is a model of the

human trisomy 21 (Down syndrome). Here we

demonstrate that cultured hippocampal neurons

from trisomy 16 mouse exhibit decreased GSH

levels and augmented cell death when compared to

diploid cells. Additional lowering of GSH levels

led to enhanced cell death in trisomy 16 cells.

Based on these results we suggest that a GSH

level which is decreased under a specific

threshold by increased consumption, reduced

synthesis or lack in precursor contributes to

cell loss and neurodegeneration in Down syndrome.

Evaluation of superoxide dismutase and

glutathione peroxidase enzymes and their

cofactors in Egyptian children with Down's syndrome.

Department of Human Genetics, National Research Centre, Cairo, Egypt.

The present work investigated the activity of

Cu/Zn superoxide dismutase enzyme (SOD) in red

blood cells and glutathione peroxidase enzyme

(GPx) in whole blood by spectrophotometric

methods. Plasma levels of the cofactors copper

and zinc and whole-blood selenium were evaluated

using atomic absorption spectrophotometer. The

study included a population of 18 Down's syndrome

(DS) patients with complete trisomy 21 (group 1),

translocations (group 2), and mosaicism (group

3), and their 15 matched controls. The purpose of

this work was to study the gene dosage effect of

SOD and its consequence on GPx enzyme and the

various cofactors, and to find out correlations

with developmental fields. Our results showed

that in the population with complete trisomy 21

and translocations, SOD and GPx activities were

increased, whereas in cases with mosaicism, the

enzymes activities were within normal limits.

Plasma copper concentrations were increased,

whereas whole-blood selenium concentrations were

significantly decreased in the three DS groups.

Plasma zinc levels were within normal in all

patients. We concluded that changes in trace

elements and enzyme activities were not related

to age or sex. Also, there was no correlation

between the enzyme levels and the developmental

activities. Our results are useful tools for

identifying nutritional status and guiding antioxidant intervention.

Correlations of glutathione peroxidase activity

with memory impairment in adults with Down syndrome.

Department of Neuroscience, University of California, San Diego, USA.

BACKGROUND: Down syndrome (DS) is a genetic

disorder (trisomy 21 in 96% of cases), associated

with an excess of a key enzyme involved with free

radical metabolism (FRM), superoxide dismutase-1

(SOD-1), that is encoded by a gene on chromosome

21. Consequently, SOD-1 activity is elevated in

DS, which also occurs in conditions of oxidative

stress, and is associated with a compensatory

increase in glutathione peroxidase activity

(GSHPx). METHODS: This study examined the

relationship of memory function with erythrocyte

SOD-1, GSHPx and catalase (CAT) activity in 22-51

year old adults with DS. RESULTS: Mean

erythrocyte SOD-1 (p < .02) and GSHPx (p < .01),

but not CAT (p = .76), activities were

significantly greater in the DS group than the

controls. In the DS group, erythrocyte GSHPx, but

not SOD-1 or CAT activities, was significantly

correlated with memory function (r = .625, p <

..025, df = 13 for savings score, r = .631, p <

..01, df = 14 for intrusion errors) but not with

intelligence quotients. CONCLUSIONS: These

observations suggest a possible relationship

between altered FRM with memory deficits among

adults with DS within the age-range in that an

age-related increase in the prevalence for

Alzheimer's neuropathology is known to be robust

before reaching a plateau of 100%.

Glutathione levels and nerve cell loss in

hippocampal cultures from trisomy 16 mouse--a model of Down syndrome.

Department of Neurophysiology, Humboldt University, Berlin, Germany.

The tripeptide glutathione (reduced state, GSH)

is an important intracellular free radical

scavenger protecting cells against oxidative

stress. The trisomy 16 mouse is a model of the

human trisomy 21 (Down syndrome). Here we

demonstrate that cultured hippocampal neurons

from trisomy 16 mouse exhibit decreased GSH

levels and augmented cell death when compared to

diploid cells. Additional lowering of GSH levels

led to enhanced cell death in trisomy 16 cells.

Based on these results we suggest that a GSH

level which is decreased under a specific

threshold by increased consumption, reduced

synthesis or lack in precursor contributes to

cell loss and neurodegeneration in Down syndrome.

Red cell superoxide dismutase, glutathione

peroxidase and catalase in Down syndrome patients

with and without manifestations of Alzheimer disease.

Department of Obstetrics and Gynaecology,

University of Toronto, Mount Sinai Hospital, Canada.

The activities of red blood cell enzymes that

scavenge the superoxide radical and hydrogen

peroxide were measured in severely to profoundly

retarded adult Down syndrome (DS) patients with

and without manifestations of Alzheimer disease

(AD), and control individuals matched for sex,

age, and time of blood sampling. Cu,Zn superoxide

dismutase (SOD-1) and glutathione peroxidase

(GSHPx) activities were significantly elevated

(1.39-fold and 1.24-fold, respectively) in DS

individuals without AD. When an adjustment was

made for the SOD gene dosage effect, DS patients

with AD manifestations had significantly lower

SOD levels than the matched control individuals.

In contrast, DS patients with and without AD had

a similar elevation in GSHPx (an adaptive

phenomenon). The mean catalase (CAT) activity was

no different in DS and control individuals;

however, in a paired regression analysis, DS

patients without AD had marginally lower CAT

activity than control individuals, whereas DS

patients with AD had slightly but not

significantly higher CAT activity. Thus, AD

manifestations in this DS population are

associated with changes in the red cell oxygen scavenging processes.

--------

Abstracts showing that Acetaminophen depletes Glutathione:

Typing in " Acetaminophen & Glutathione " in PubMed

(www.pubmed.com) brings up 54 pages of results -

lots of stuff there! Below are just several abstracts I thought were very good.

Full text at: http://www.jbc.org/cgi/content/abstract/M605143200v1

" Acetaminophen overdose is a leading cause of

drug related acute liver failure in the United

States. Glutathione, a tripeptide antioxidant

protects cells against oxidative damage from

reactive oxygen species and plays a crucial role

in the detoxification of xenobiotics, including acetaminophen. "

Acetaminophen Hepatotoxicity: An Update

Acetaminophen is a widely used nonprescription

analgesic and antipyretic agent. It is also a

dose-related hepatotoxin that can cause fulminant

liver failure when taken in massive overdoses or,

much less commonly, at therapeutic doses in

susceptible individuals. Persons who regularly

consume alcohol or persons who have been fasting

may be more susceptible to this hepatotoxicity.

This liver injury is due not to the drug itself

but to the formation of the toxic metabolite

N-acetyl-p-benzoquinine imine generated through

the cytochrome P-450 drug-metabolizing system.

Normally, hepatic stores of glutathione combine

with the toxic metabolite and prevent liver cell

injury. When glutathione stores are depleted by

overproduction of this metabolite, however, the

reactive metabolite binds to liver cell proteins

and causes hepatic necrosis. P-450 2E1 is induced

by alcohol consumption and possibly starvation,

and glutathione depletion can occur due to the

inadequate nutrition occurring in chronic alcohol

use or in starvation. Recent studies have shown

that activated Kupffer cells and their secreted

toxic agents such as cytokines may also play a

role in this liver injury. This liver injury is

characterized by extremely high levels of serum

aspartate aminotransferase (AST) and alanine

aminotransferase (ALT) (> 1000), and bad

prognostic signs include severe prolongation of

the prothrombin time, renal dysfunction, and,

most importantly, acidosis. N-acetylcysteine is a

highly effective antidote when given early

(within 15 hours) of overdose. Some patients may

develop such fulminant liver injury that they

require transplantation. Unfortunately, many such

patients have a course so rapid that a donor

liver may not become available in time. Thus,

both the medical community and the general public

require a heightened understanding of this

clinical problem in order to initiate prevention

measures and to implement early therapeutic

measures if an overdose situation occurs.

This is a really good abstract on Acetaminophen,

at what dose it depletes Glutathione, over how

long it is active, & what to give to stop that

depletion (note the bolded part at the end):

Dose-dependent pharmacokinetics of acetaminophen:

evidence of glutathione depletion in humans.

The time course of excretion of acetaminophen and

its metabolites in urine was determined in eight

healthy adults (seven men and one woman) who

ingested 1 gm of the drug and collected timed

urine samples for 24 hours. The mean time of peak

excretion rate was 1.3 to 3.7 hours for

acetaminophen, its glucuronide, sulfate,

cysteine, mercapturate, and methoxy metabolites

but 13.5 hours for methylthioacetaminophen. The

mean half-life of acetaminophen was 3.1 hours and

the mean half-life of the metabolites other than

methylthioacetaminophen ranged from 4.1 to 5.7

hours. The half-life of methylthiometabolite

could not be determined because of its very late

peak time. In a second study the effect of dose

on the clearance of acetaminophen was determined

in nine healthy adult subjects (eight men and one

woman) who received doses of 0.5 and 3 gm

acetaminophen on separate occasions, separated by

4 to 10 days. The renal clearance of

acetaminophen and the formation clearances of the

sulfate, glutathione, and catechol metabolites

were lower (by 38%, 41%, 35%, and 46%,

respectively) at the higher dose. The renal

clearance of acetaminophen sulfate and

glucuronide conjugates were not different between

doses. In a third study (10 men), 10 gm

N-acetylcysteine was found to increase the

formation clearance of the sulfate conjugate by

27% and that of the glutathione conjugate by 10%.

The data suggest that the hepatic supply of

reduced glutathione and 3'-phosphoadenosine

5'-phosphosulfate begins to be depleted over the

range of 0.5 to 3 gm acetaminophen and that the

depletion is overcome by the administration of N-acetylcysteine.

The below abstract is also a very good abstract

talking about GSH & different drugs (particularly Acetaminophen):

Therapeutic doses of acetaminophen stimulate the

turnover of cysteine and glutathione in man.

In spite of the importance of glutathione (GSH)

in the detoxification of toxic metabolites of

drugs, virtually nothing is known about the

regulation of hepatic GSH homeostasis in man. In

order to estimate the turnover of hepatic GSH and

to assess the effect of different doses of

acetaminophen (paracetamol) on the synthesis of

GSH in man, [3H]cystine and varying doses of

acetaminophen were administered to healthy

volunteers, and the time course of the specific

activity of the cysteine moiety of

N-acetylcysteinyl-acetaminophen excreted in urine

was followed. The fractional rate of turnover of

the tracer in N-acetylcysteinyl-acetaminophen

increased significantly from 0.031 +/- 0.007 h-1

after doses of acetaminophen ranging from 50 to

300 mg to 0.045 +/- 0.011 and 0.121 +/- 0.027 h-1

following 600 and 1200 mg of acetaminophen,

respectively. The data indicate that therapeutic

doses of acetaminophen markedly stimulate the

rate of turnover of the pool of cysteine

available for the synthesis of GSH, most likely

due to an increased rate of synthesis of GSH

which is required to detoxify the toxic

metabolite of acetaminophen. Patients who are not

able to respond to a similar demand on their

stores of GSH by increasing the synthesis of GSH

may be at higher risk of developing hepatic

injury from drugs that require GSH for their detoxification.

Paracetamol:

" Conclusions In febrile children, treatment with

repeated supratherapeutic doses of paracetamol is

associated with reduced antioxidant status and

erythrocyte glutathione concentrations. These

significant changes may indicate an increased

risk for hepatotoxicity and liver damage. "

Abstract at:

http://www.blackwell-synergy.com/doi/abs/10.1046/j.1365-2125.2003.01723.x

Glutathione & Thimerosal Neurotoxicity:

This abstract says that Glutathione can defend

against Thimerosal neurotoxicity. This study was

done on children who do not have DS, therefore,

it would make the case all the more to not give a

child with Down Syndrome Acetaminophen if he has

been vaccinated recently. Also, it would be

beneficial to give a child with Down Syndrome

extra Glutathione if they are being vaccinated,

to help prevent neurotoxicity from Thimerosal -

since their levels of Glutathione are

diminished, they would have a potentally greater

risk of having neurotoxicity from Thimerosal if

they are not supplemented with Glutathione.

Thimerosal neurotoxicity is associated with

glutathione depletion: protection with glutathione precursors.

Department of Pediatrics, University of Arkansas

for Medical Sciences and Arkansas Children's

Hospital Research Institute, Little Rock, AR 72202, USA. jamesjill@...

Thimerosol is an antiseptic containing 49.5%

ethyl mercury that has been used for years as a

preservative in many infant vaccines and in flu

vaccines. Environmental methyl mercury has been

shown to be highly neurotoxic, especially to the

developing brain. Because mercury has a high

affinity for thiol (sulfhydryl (-SH)) groups, the

thiol-containing antioxidant, glutathione (GSH),

provides the major intracellular defense against

mercury-induced neurotoxicity. Cultured

neuroblastoma cells were found to have lower

levels of GSH and increased sensitivity to

thimerosol toxicity compared to glioblastoma

cells that have higher basal levels of

intracellular GSH. Thimerosal-induced

cytotoxicity was associated with depletion of

intracellular GSH in both cell lines.

Pretreatment with 100 microM glutathione ethyl

ester or N-acetylcysteine (NAC), but not

methionine, resulted in a significant increase in

intracellular GSH in both cell types. Further,

pretreatment of the cells with glutathione ethyl

ester or NAC prevented cytotoxicity with exposure

to 15 microM Thimerosal. Although Thimerosal has

been recently removed from most children's

vaccines, it is still present in flu vaccines

given to pregnant women, the elderly, and to

children in developing countries. The potential

protective effect of GSH or NAC against mercury

toxicity warrants further research as possible

adjunct therapy to individuals still receiving

Thimerosal-containing vaccinations.

Full text at: http://www.icdrc.org/pdf/Neurotoxarticle.pdf

Home

[Guest guest]

Thank you for this post, Sheri. This information really clears up

some questions I had.

As I was reading through this info, I remembered that a few years ago

a friend of mine was studying to be a pharmacist. We were at the

bowling alley getting ready to bowl on our league and I (at the time a

VERY BUSY real estate agent) had a horrible headache after a

particularly bad day. I asked the front desk for the bottle of

Tylenol, Extra Strength - which they share freely to any bowler that

frequents the place - and proceeded to state that I was going to take

an extra capsule because my headache was so bad. My friend was

standing next to me and he put his hand over the cap of the bottle to

prevent me from opening it. His EXACT words, which I will never

forget were, " Even ONE of those can kill you. Please reconsider and

don't take that. " He also told me that after he learned about

acetaminophen and other pain relievers in his class, he just preferred

to let his body work through the little nuisance aches and pains.

That spoke volumes to me; if someone who going to school to learn how

to dish out drugs like candy is afraid to take it himself, why on

earth would ANYONE want to take it? I haven't touched any OTC pain

relievers since that day - only homeopathy.

On Tue, Jul 29, 2008 at 8:56 AM, Sheri Nakken <vaccineinfo@...> wrote:

> your liver is already taxed in illness and

> working overtime. Add insult to injury by making

> it detox tylenol which is so very hard on the liver