Prev: TAKE YOUR FREE TIPS FOR HEALTH FROM NUTRITION
Next: Aneurysm and Multiple Sclerosis
From: ironjustice on 8 Aug 2008 09:32
Increased oxidative stress suggested by low serum vitamin E
concentrations in patients with chronic fatigue syndrome.
Miwa K, Fujita M
Int J Cardiol 2008 Aug 4.

Serum alpha-tocopherol concentrations were determined in 50 patients
with chronic fatigue syndrome (CFS) and 40 control subjects (Control).
Prevalence of each or any coronary risk factor was not significantly
different between CFS and Control. CFS had significantly lower alpha-
tocopherol concentrations than Control. The concentrations were
significantly lower in the subjects with any coronary risk factors
than those without in CFS as well as Control. Even among the subjects
with any coronary risk factors and also among those without, CFS had
significantly lower alpha-tocopherol concentrations than Control. In
conclusion, CFS had significantly lower alpha-tocopherol
concentrations irrespective of coronary risk factors than Control,
suggesting the presence of increased oxidative stress in CFS.


International journal of cardiology [Int J Cardiol]


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


Who loves ya.
Tom


Jesus Was A Vegetarian!
http://tinyurl.com/2r2nkh


Man Is A Herbivore!
http://tinyurl.com/4rq595


DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk
From: jay on 8 Aug 2008 16:21
> Increased oxidative stress suggested by low serum vitamin E
> concentrations in patients with chronic fatigue syndrome.
> In conclusion, CFS had significantly lower alpha-tocopherol
> concentrations irrespective of coronary risk factors than Control,
> suggesting the presence of increased oxidative stress in CFS.

Chronic Fatigue Syndrome can have multiple causes. One of them can be
Persistent Organic Pollutants (POPs), and more specifically, TCDD, a
potent dioxin. It bioaccumlates and biomagnifies up the food chain.
Most people have gotten / are getting TCDD from consumption of meat/
fish/poultry/egg/dairy fats during the past three decades. Even with
TCDD levels decreasing in dietary fats, people's level are still
rising because it takes 10 years to eliminate half of what you have
today, assuming you are not being exposed to anymore, which is not the
case. Because TCDD is highly lipophilic, it accumulate in fatty body
tissues, including the nervous system. TCDD binds with cell's Aryl
Hydrocarbon Receptor and activates detoxification enzymes. These detox
enzymes aren't able to detox TCDD. Experiments suggests that the detox
enzymes end up binding with other compounds (ie endogenous estrogens,
exogenous estrogen-like compounds, POPs) and create toxic
intermediates, free radicals, DNA damage and cancer.

The number of pathologies initiated by inappropriate activation of the
AhR-mediated pathways is mind boggling. Pharmaceuticals usually drop a
drug from further research, if it activates the AhR-mediated pathways.


Induction of Oxidative Stress Responses by Dioxin and other Ligands of
the Aryl Hydrocarbon Receptor.
TCDD and other polyhalogenated aromatic hydrocarbon ligands of the
aryl hydrocarbon receptor (AHR) have been classically considered as
non-genotoxic compounds because they fail to be directly mutagenic in
either bacteria or most in vitro assay systems. They do so in spite of
having repeatedly been linked to oxidative stress and to mutagenic and
carcinogenic outcomes. Oxidative stress, on the other hand, has been
used as a marker for the toxicity of dioxin and its congeners. We have
focused this review on the connection between oxidative stress
induction and the toxic effects of fetal and adult dioxin exposure,
with emphasis on the large species difference in sensitivity to this
agent. We examine the roles that the dioxin-inducible cytochromes
P450s play in the cellular and toxicological consequences of dioxin
exposure with emphasis on oxidative stress involvement. Many
components of the health consequences resulting from dioxin exposure
may be attributable to epigenetic mechanisms arising from prolonged
reactive oxygen generation. PMID: 18648615


The modulatory effects of ellagic acid and vitamin E succinate on TCDD-
induced oxidative stress in different brain regions of rats after
subchronic exposure.
The effects of ellagic acid (EA) and vitamin E succinate (VES) on
2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced oxidative stress in
different brain regions of rats have been studied after subchronic
exposure to the compounds. TCDD was administered to groups of rats at
a dose of 46 ng/kg/day for 90 days. EA and VES were administered to
groups of rats, either separately or simultaneously with TCDD, every
other day for 90 days. At the end of the treatment period, animals
were sacrificed and brains were dissected to cerebral cortex (Cc),
hippocampus (H), cerebellum (C), and brain stem (Bs), and were assayed
for production of superoxide anion (SA), lipid peroxidation (LP), and
DNA single-strand breaks (SSBs). While TCDD administration to rats
resulted in significant production of SA, LP, and DNA SSBs in Cc and
H, simultaneous administration of VES or EA with the xenobiotics
resulted in significant protection against those effects. The results
also indicate that VES provided a better protyection against TCDD-
induced effects in brains when compared with EA. PMID: 15452880


Relationship between clinical features and blood levels of
pentachlorodibenzofuran in patients with Yusho.
BACKGROUND: Yusho is a form of food poisoning that occurred in 1968,
as a result of consuming rice bran oil contaminated with
polychlorinated biphenyls (PCBs) and various dioxins such as
polychlorinated dibenzofurans (PCDFs). The victims of Yusho suffered
from various dermatological, ophthalmological, and mucosal symptoms in
addition to general FATIGUE, weight loss, anorexia, headache,
paresthesia of the extremities, abdominal pain, cough and sputa,
dysmenorrhea, and growth retardation in infants and children. We
measured the blood levels of dioxins in the annual medical check-up of
Yusho patients from 2001 to 2003. PURPOSE: To analyze the relationship
between the concentrations of PCDFs/PCBs and the subjective/objective/
laboratory findings of patients with Yusho. We also compared the
present clinical findings with those collected in 1988. RESULTS AND
DISCUSSION: The mean blood level of 2,3,4,7,8-pentachlorodibenzofuran
(PeCDF) in 359 patients with Yusho was 177.50 pg/g lipids, which was
much higher than that of normal controls (15.2 +/- 8.9 pg/g lipids).
The blood levels of PeCDF were significantly correlated with total PCB
levels, hexachlorobiphenyl levels, urinary sugar, 2-h erythrocyte
sedimentation rate, thymol turbidity test, and sodium levels. A
significant correlation was also noted with dermatological findings
(acneform eruption and comedones), mucosal findings (oral
pigmentation), constipation, numbness in the extremities, body weight
loss, and abnormal abdominal ultrasonography. The incidence and
severity of most of the dermatological and ophthalmological symptoms
decreased from 1988 to 2001-2003. In conclusion, high amounts of PCBs
and PeCDF are still present in a number of patients with Yusho. The
patients still suffer from various mucocutaneous and subjective
symptoms. PMID: 17366567


External Qi therapy to treat symptoms of Agent Orange Sequelae in
Korean combat veterans of the Vietnam War.
We investigated the efficacy of Qi therapy as a non-pharmacological
treatment for various symptoms presented by Korean combat veterans of
the Vietnam War with Agent Orange Sequelae. Nine subjects volunteered
to receive 30 minutes of Qi therapy, twice per day for 7 days. There
was marked improvement in 89% of the patients with impaired physical
activity, 86% of those with psychological disorder, 78% of those with
heavy drug use, and 67% of those with FATIGUE, indigestion and high
blood glucose levels. This data suggests that Qi therapy combined with
conventional treatment has positive effects in reducing and managing
the pain, psychosomatic disorders, and substance abuse in patients
with Agent Orange Sequelae. We cannot completely discount the possible
influence of the placebo effect, and more objective, clinical measures
are needed to study the long-term effects of Qi therapy. PMID:
15344429


Dystonia and tremor following exposure to 2,3,7,8-tetrachlorodibenzo-p-
dioxin.
Forty-seven railroad workers who were exposed to polychlorinated
phenols, including dioxin (TCDD), during 1979 while cleaning up the
chemical spillage following damage to a tank car filled with these
chemicals were followed medically for the subsequent 6 years. Two
committed suicide. The initial neurological complaints included a
sense of FATIGUE and muscle aching, both of which have been reported
in other individuals following dioxin exposure. On detailed
neurological examination in December, 1985, 24 of 45 had dystonic
writer's cramp and/or other action dystonias of the hands. None of the
involved individuals had a family history of dystonia, and all 24
dated the onset of the dystonia to the first 2 to 3 years subsequent
to their toxic exposure. The dystonias varied in severity but were
usually mild. No other types of dystonic involvement were recognized.
Thirty-five of the 45 individuals also manifested postural and
terminal intention tremor which resembled benign essential tremor.
None of the involved individuals had a family history of tremor, and
all 35 of those affected dated the onset of the tremor to some time
subsequent to their toxic exposure. Forty-three of 45 patients had
histories and findings suggestive of peripheral neuropathy. This is
the first report relating any type of dystonia to prior dioxin
exposure and the first report relating action dystonia, such as
dystonic writer's cramp, and postural/terminal intention tremor, to
toxic exposure of any type. PMID: 2849055


Commentary on 2,3,7,8-tetrachlorodibenzo-para-dioxin (TCDD).
There is deep concern about the long term health effects of exposure
to phenoxy herbicides and the contaminant TCDD; however, there is
considerable scientific and medical uncertainty regarding the health
effects from exposure to these chemicals. There are at least ten
ongoing studies on reproduction, morbidity and mortality as well as
studies of tissue concentrations of TCDD that are attempting to
determine the health effects of these chemicals (see Table 2).
Appropriate efforts should be made to prevent human and environmental
exposure and to decontaminate the environment while awaiting the
results of these investigations. Animal toxicity studies show such
wide variations that extrapolations from a different species to humans
are tenuous. Human studies on exposed workers and nonoccupational
exposures are difficult to interpret because the exposure has not been
quantified and because workers were exposed to mixtures of chemicals.
Chloracne appears to be an important specific clinical marker of TCDD
exposure, however, it can be caused by structurally similar compounds.
Many of the past studies on human health effects of 2,4,5-T and TCDD
are controversial. Since the scientific data are not firm, no specific
statements can be made regarding the long term health effects at this
time. Any individual who has had a significant exposure to TCDD should
see his/her physician and have appropriate consultation. Long term
follow up will be required. Physicians should be instructed regarding
the possible manifestations of TCDD exposure to look for chloracne,
soft tissue masses, muscle pain, FATIGUE, peripheral neuropathy,
tender hepatic enlargement, enlargement, elevated liver enzymes,
elevated lipids, prolonged prothrombin time, hemorrhagic cystitis and
hirsutism, PMID: 4060565
From: ironjustice on 8 Aug 2008 16:56
On Aug 8, 6:32 am, ironjustice <teamtan...(a)hotmail.com> wrote:
Increased oxidative stress suggested by low serum vitamin E
concentrations in patients with chronic fatigue syndrome. <<

Fatigue .. overwhelming fatigue when one gets hemolysis ..

You treat the hemolysis and the fatigue is cured.

Lack of vitamin E .. causes .. hemolysis ..

When you give vitamin E to a person who HAS hemolysis and vitamin E
deficiency .. ?

They are .. cured ..

Hemolytic anemia ..

Cites for all .. of the above ..


Who loves ya.
Tom


Jesus Was A Vegetarian!
http://tinyurl.com/2r2nkh


Man Is A Herbivore!
http://tinyurl.com/4rq595


DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk



> Miwa K, Fujita M
> Int J Cardiol 2008 Aug 4.
>
> Serum alpha-tocopherol concentrations were determined in 50 patients
> with chronic fatigue syndrome (CFS) and 40 control subjects (Control).
> Prevalence of each or any coronary risk factor was not significantly
> different between CFS and Control. CFS had significantly lower alpha-
> tocopherol concentrations than Control. The concentrations were
> significantly lower in the subjects with any coronary risk factors
> than those without in CFS as well as Control. Even among the subjects
> with any coronary risk factors and also among those without, CFS had
> significantly lower alpha-tocopherol concentrations than Control. In
> conclusion, CFS had significantly lower alpha-tocopherol
> concentrations irrespective of coronary risk factors than Control,
> suggesting the presence of increased oxidative stress in CFS.
>
> International journal of cardiology [Int J Cardiol]
>
> ---------------------------------------------------------------------------­-----
>
> Who loves ya.
> Tom
>
> Jesus Was A Vegetarian!http://tinyurl.com/2r2nkh
>
> Man Is A Herbivore!http://tinyurl.com/4rq595
>
> DEAD PEOPLE WALKINGhttp://tinyurl.com/zk9fk

From: jay on 8 Aug 2008 17:26
> Fatigue .. overwhelming fatigue when one gets hemolysis ..
> You treat the hemolysis and the fatigue is cured.
> Lack of vitamin E .. causes .. hemolysis ..
> When you give vitamin E to a person who HAS hemolysis
> and vitamin E deficiency .. ?
> They are .. cured ..


Hemolysis is the breaking open of red blood cells and the release of
hemoglobin into the surrounding fluid (plasma, in vivo).

Erythrocytes - red blood cells.


Damage to erythrocytes caused by 2,3,7,8-tetrachloro-dibenzo-p-dioxin
(in vitro).
The effects of the exposure of human erythrocytes to different
concentrations of 2,3,7,8-tetrachlorodibenzo-p-dioxin were studied.
Particular attention was paid to lipid peroxidation, haemoglobin
oxidation, and changes in the activity of catalase and glutathione
peroxidase. Human erythrocytes at a 5% haematocrit were incubated with
2,3,7,8-TCDD at concentrations of 0.2 ppm to 1.6 ppm (ng-microg/ml
erythrocytes) for 1 hour. The results obtained show that 2,3,7,8-TCDD
induces the generation of lipid peroxides and the oxidation of Hb, and
decreases the activity of catalase and glutathione peroxidase. This
supports the thesis that TCDD causes oxidative stress in erythrocytes.
PMID: 15213807


Interaction of 2,4-dichlorophenoxyacetic acid (2,4-D) with cell and
model membranes.
2,4-dichlorophenoxyacetic acid (2,4-D), a widely used herbicide, is a
component of the "agent orange' whose toxicity has been extensively
studied without definite conclusions. In order to evaluate its
perturbing effect upon cell membranes, 2,4-D was made to interact with
human erythrocytes and molecular models. These studies were performed
by scanning electron microscopy on red cells, fluorescence
spectroscopy on dimyristoylphosphatidylcholine (DMPC) large
unilamellar vesicles and X-ray diffraction on multilayers of DMPC and
dimyristoylphosphatidylethanolamine (DMPE). It was observed that 2,4-D
induced a pronounced shape change to the erythrocytes. This effect is
explained by the herbicide interaction with the outer monolayer of the
red cell membrane. PMID: 8972711


Microarray analysis of gene expression in peripheral blood mononuclear
cells from dioxin-exposed human subjects.
Tetrachlorodibenzo-p-dioxin (TCDD) is classified as a human carcinogen
and exerts toxic effects on the skin (chloracne). Effects on
reproductive, immunological, and endocrine systems have also been
observed in animal models. TCDD acts through the aryl hydrocarbon
receptor (AhR) pathway influencing largely unknown gene networks. An
industrial accident in Seveso, Italy in 1976 exposed thousands of
people to substantial quantities of TCDD. Twenty years after the
exposure, this study examines global gene expression in the
mononuclear cells of 26 Seveso female never smokers, with similar age,
alcohol consumption, use of medications, and background plasma levels
of 22 dioxin congeners unrelated to the Seveso accident. Plasma dioxin
levels were still elevated in the exposed subjects. We performed
analyses in two different comparison groups. The first included high-
exposed study subjects compared with individuals with background TCDD
levels (average plasma levels 99.4 and 6.7ppt, respectively); the
second compared subjects who developed chloracne after the accident,
and those who did not develop this disease. Overall, we observed a
modest alteration of gene expression based on dioxin levels or on
chloracne status. In the comparison between high levels and background
levels of TCDD, four histone genes were up-regulated and modified
expression of HIST1H3H was confirmed by real-time PCR. In the
comparison between chloracne case-control subjects, five hemoglobin
genes were up-regulated. Pathway analysis revealed two major networks
for each comparison, involving cell proliferation, apoptosis,
immunological and hematological disease, and other pathways. Further
examination of the role of these genes in dioxin induced-toxicity is
warranted. PMID: 17101203


Influence of aromatic hydrocarbon receptor-mediated events on the
genotoxicity of cigarette smoke condensate.
The role of aromatic hydrocarbon receptor (AhR)-mediated events on the
genotoxicity of mainstream cigarette smoke condensate was
investigated. Together, these data suggest that cigarette smoke
contains chemicals which transform the AhR to an active transcription
factor and AhR-regulated enzyme induction plays an important role in
mediating the genotoxicity of this complex environmental pollutant.
PMID: 9855021
From: ironjustice on 8 Aug 2008 19:59
On Aug 8, 2:26 pm, jay <jaym1...(a)hotmail.com> wrote:2,3,7,8-
tetrachloro-dibenzo-p-dioxin <<

Maybe what you should dooo .. is give us a cite for this .. removal of
2,3,7,8-tetrachloro-dibenzo-p-dioxin .. curing .. anemia .. ?

You have an article for that .. ?

How about dioxin .. depleting .. tocopherol .. ?

You have an article for that .. ?

You seem to be posting pretty much the same articles .. over and
over ..

Who loves ya.
Tom


Jesus Was A Vegetarian!
http://tinyurl.com/2r2nkh


Man Is A Herbivore!
http://tinyurl.com/4rq595


DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk



> > Fatigue .. overwhelming fatigue when one gets hemolysis ..
> > You treat the hemolysis and the fatigue is cured.
> > Lack of vitamin E .. causes .. hemolysis ..
> > When you give vitamin E to a person who HAS hemolysis
> > and vitamin E deficiency .. ?
> > They are .. cured ..
>
> Hemolysis is the breaking open of red blood cells and the release of
> hemoglobin into the surrounding fluid (plasma, in vivo).
>
> Erythrocytes - red blood cells.
>
> Damage to erythrocytes caused by 2,3,7,8-tetrachloro-dibenzo-p-dioxin
> (in vitro).
> The effects of the exposure of human erythrocytes to different
> concentrations of 2,3,7,8-tetrachlorodibenzo-p-dioxin were studied.
> Particular attention was paid to lipid peroxidation, haemoglobin
> oxidation, and changes in the activity of catalase and glutathione
> peroxidase. Human erythrocytes at a 5% haematocrit were incubated with
> 2,3,7,8-TCDD at concentrations of 0.2 ppm to 1.6 ppm (ng-microg/ml
> erythrocytes) for 1 hour. The results obtained show that 2,3,7,8-TCDD
> induces the generation of lipid peroxides and the oxidation of Hb, and
> decreases the activity of catalase and glutathione peroxidase. This
> supports the thesis that TCDD causes oxidative stress in erythrocytes.
> PMID: 15213807
>
> Interaction of 2,4-dichlorophenoxyacetic acid (2,4-D) with cell and
> model membranes.
> 2,4-dichlorophenoxyacetic acid (2,4-D), a widely used herbicide, is a
> component of the "agent orange' whose toxicity has been extensively
> studied without definite conclusions. In order to evaluate its
> perturbing effect upon cell membranes, 2,4-D was made to interact with
> human erythrocytes and molecular models. These studies were performed
> by scanning electron microscopy on red cells, fluorescence
> spectroscopy on dimyristoylphosphatidylcholine (DMPC) large
> unilamellar vesicles and X-ray diffraction on multilayers of DMPC and
> dimyristoylphosphatidylethanolamine (DMPE). It was observed that 2,4-D
> induced a pronounced shape change to the erythrocytes. This effect is
> explained by the herbicide interaction with the outer monolayer of the
> red cell membrane. PMID: 8972711
>
> Microarray analysis of gene expression in peripheral blood mononuclear
> cells from dioxin-exposed human subjects.
> Tetrachlorodibenzo-p-dioxin (TCDD) is classified as a human carcinogen
> and exerts toxic effects on the skin (chloracne). Effects on
> reproductive, immunological, and endocrine systems have also been
> observed in animal models. TCDD acts through the aryl hydrocarbon
> receptor (AhR) pathway influencing largely unknown gene networks. An
> industrial accident in Seveso, Italy in 1976 exposed thousands of
> people to substantial quantities of TCDD. Twenty years after the
> exposure, this study examines global gene expression in the
> mononuclear cells of 26 Seveso female never smokers, with similar age,
> alcohol consumption, use of medications, and background plasma levels
> of 22 dioxin congeners unrelated to the Seveso accident. Plasma dioxin
> levels were still elevated in the exposed subjects. We performed
> analyses in two different comparison groups. The first included high-
> exposed study subjects compared with individuals with background TCDD
> levels (average plasma levels 99.4 and 6.7ppt, respectively); the
> second compared subjects who developed chloracne after the accident,
> and those who did not develop this disease. Overall, we observed a
> modest alteration of gene expression based on dioxin levels or on
> chloracne status. In the comparison between high levels and background
> levels of TCDD, four histone genes were up-regulated and modified
> expression of HIST1H3H was confirmed by real-time PCR. In the
> comparison between chloracne case-control subjects, five hemoglobin
> genes were up-regulated. Pathway analysis revealed two major networks
> for each comparison, involving cell proliferation, apoptosis,
> immunological and hematological disease, and other pathways. Further
> examination of the role of these genes in dioxin induced-toxicity is
> warranted. PMID: 17101203
>
> Influence of aromatic hydrocarbon receptor-mediated events on the
> genotoxicity of cigarette smoke condensate.
> The role of aromatic hydrocarbon receptor (AhR)-mediated events on the
> genotoxicity of mainstream cigarette smoke condensate was
> investigated. Together, these data suggest that cigarette smoke
> contains chemicals which transform the AhR to an active transcription
> factor and AhR-regulated enzyme induction plays an important role in
> mediating the genotoxicity of this complex environmental pollutant.
> PMID: 9855021

 |  Next  |  Last
Pages: 1 2
Prev: TAKE YOUR FREE TIPS FOR HEALTH FROM NUTRITION
Next: Aneurysm and Multiple Sclerosis