Re: Sorry for what my company did

[Guest guest]

no company cares about its employees. they only care about the bottom line and

how much profit they make in a year. it means bigger bonus checks for the ceo

and the directors. you can't control what they do so you shouldn't apologize for

their greed. i work for a national discount chain and it doesn't care about

anything but profit.

marcusdouglashorton <marcusdouglashorton@...> wrote: Hello,

Safeway went to court against the state of Ca when the state of

Ca just asked Safeway to put warning labels on fish items that stated

that this product contains chemicals which can cause cancer and birth

defects. In fact Safeway got the federal government to state that

one can find no scientific reason for the state of Ca to ask Safeway

or other companies to put warning labels on fish items. This not

true and I would like to apologized for the actions of the company I

work for. I was once a biology major and I have done a scientific

literature search and I found out that what Safeway and the federal

government stated is not true. I will show you the exact opposite is

true and I have decided to show how mercury can cause human cancer.

I will include copies of science abstracts so that you can see that I

am not making things up. I think I should state before I go on that

it is methylmercury cysteine that is found in fish (Sience 29 August

2003) and that the human body makes methylmercury chloride out of

that form. Also that inside the human body methylmercury chloride

loses its functional groups so that one can find various other forms

of mercury including just plain mercury in the human body.

To begin with we have known since at least 1982 that mercury

binds to the DNA. Next we have known since at least 1993 that the

wild (normal) type of p53 gene is mutated. Mutation of this gene is

associated with various types of cancers. Since at least 1997 we

have known that mercury chloride cause gene overexpression of the c-

fos gene which also occurs in various types of cancers. Another

cancer gene that mercury has an impact on is the jun gene and we have

known that from at least 2000. Chromosomal abnormalities are

associated with cancers. In fact that is one of theories of how

cancer starts. We have known for decades that methymercury and other

mercury compounds can cause that. In fact we have population studies

that show blood cells have DNA damage due to people exposed to

mercury compounds including methylmercury. We also have population

studies which show areas that had methylmercury poisoning had higher

cancer rates. All the poisoning did was show that methylmercury is

one of the factors in the normal cancer rate of cancer. One has to

push out something from the normal rate in order to see it. The

normal rate includes all factors that cause cancer so how do you know

what causes cancer unless one pushes it out.

This is just some of the things I know. All of this and more

was known before Safeway and the state of Ca went to court on the

issue of putting warning labels on fish items. I am sorry that

Safeway did not state the truth on this matter. Please take my

apology on this matter since the company I work for does not care for

the health and well being of its customers.

Marcus Horton

Safeway division 12 store 0706

Tishaart@...

: Biochemistry. 1982 Jan 5;21(1):62-6. Links

Binding of mercury(II) to poly(dA-dT) studied by proton nuclear

magnetic resonance.

Young PR, Nandi US, Kallenbach NR.

The binding of Hg(II) to poly(dA-dT) has been examined with proton

NMR spectroscopy. Addition of HgCl2 between r (Hg2+/nucleotide) = 0

and 0.25 results in loss of the exchangeable imino N3H resonance of

thymine, indicating preferential binding at this site. The

nonexchangeable base resonances AH8, AH2, and TH6 shift their

intensity downfield in a cooperative manner, indicating complexation

which is slow on the NMR time scale and changes in the polymer

conformation upon binding. At r = 0.25, the polymer is cross-linked,

and an increase in temperature does not result in denaturation of the

polymer, as evidenced by the thymine proton resonance chemical

shifts. The chemical shifts of the AH2 and T(CH3)5 base resonances

allow some general conclusions to be made about the stereochemistry

of this complex

1: Inorg Chem. 1996 Sep 11;35(19):5654-5662. Links

Mercury(II) Site-Selective Binding to a DNA Hairpin. Relationship of

Sequence-Dependent Intra- and Interstrand Cross-Linking to the

Hairpin-Duplex Conformational Transition.

Kuklenyik Z, Marzilli LG.

Department of Chemistry, Emory University, Atlanta, Georgia 30322.

Hg(II) interacted site selectively with only one of three

deoxyribooligonucleotides examined; these " oligos " each had a

different number of unmatched T residues. Thus, Hg(II) formed an

intrastrand T-Hg-T cross-link between the first and fourth T residues

of the hairpin, d(GCGCTTTTGCGC) (T4). The DNA strand formed a loop

around the Hg, as if the Hg atom had been lassoed. The interactions

of Hg(II) with two other oligos, d(ATGGGTTCCCAT) (T2) and d

(GCGCTTTGCGC) (T3), were less specific. Previously, we found that at

high DNA and salt concentrations, T2 was a mixture of hairpin and

duplex forms while T3 and T4 had the hairpin form; modeling studies

showed that in the free T4 hairpin the two T's at the ends of the (T)

(4) loop form a T.T wobble base pair. Only in T4 are the T residues

positioned to form an intrastrand cross-link readily. The Hg(II)-

oligo adducts formed as a function of added Hg(II) were investigated

by titrations monitored by UV, CD, and (1)H NMR spectroscopy. The

appearance of a new set of (1)H signals with the concomitant decay of

the free oligo (1)H signals indicated that 1:1 Hg(II):T2, 1.5:1 Hg

(II):T3, and 1:1 Hg(II):T4 adducts were formed with Hg(NO(3))(2). In H

(2)O, these adducts all had spectra with very downfield signals for

the exchangeable TN(3)H and GN(1)H groups, a characteristic of base-

paired regions. All upfield N(3)H signals from the (T)(2) and (T)(3)

sequences of the free oligo disappeared in the spectra of the 1:1 Hg

(II):T2 and 1.5:1 Hg(II):T3 adducts. The disappearance of the NH

signals, the UV spectral changes, and the stoichiometries (1:1 Hg

(II):T2 and 1.5:1 Hg(II):T3) indicate that these adducts are duplexes

containing two and three T-Hg-T interstrand cross-links for T2 and

T3, respectively. The (1)H and (13)C signals of the 1:1 Hg(II):T4

adduct in D(2)O were nearly completely assigned by 2D NMR

spectroscopy. The spectrum of the adduct in H(2)O had only two of the

four original TN(3)H signals from the (T)(4) sequence present in the

spectrum of T4; this result is consistent with the presence of a TN3-

Hg-TN3 cross-link. The (13)C chemical shift changes upon Hg(II)

binding indicated that the TN3-Hg-TN3 cross-link was between the T's

at each end of the (T)(4) loop. The NOESY, CD, and UV spectra were

all consistent with a hairpin conformation for the 1:1 Hg(II):T4

adduct. A hairpin conformation also appeared reasonable from

molecular modeling calculations. In conclusion, the length of the

central (T)(n)() sequence influenced the type of T-Hg-T cross-link

formed and, in turn, the conformation of the adducts. For (T)(2) and

(T)(3), interstrand T-Hg-T cross-linking favored the duplex form. In

contrast, for (T)(4), intrastrand T-Hg-T cross-linking stabilized the

hairpin form.

1: Cancer Res. 1993 Apr 15;53(8):1739-42. Links

A structural role for metal ions in the " wild-type " conformation of

the tumor suppressor protein p53.

Hainaut P, Milner J.

Department of Biology, University of York, Heslington, United Kingdom.

In human tumors, many different point mutations of the p53 gene knock

out suppressor function and induce the p53 polypeptide to adopt an

immunologically distinct, " mutant " conformation. Here we show that

exposure to the metal chelator 1,10-phenanthroline induces wild-type

p53 to adopt the mutant conformation and that this process is

reversible. Conversion to mutant phenotype also occurs after exposure

to (a) an organic mercurial reagent targeting cysteinyl residues and

( low concentrations of mercury or cadmium. We propose that binding

of metal ions, most probably zinc, to conserved cysteinyl residues

stabilizes the tertiary structure of wild-type p53.

1: Chem Biol Interact. 1997 Dec 12;108(1-2):95-106. Links

Induction of c-fos gene by mercury chloride in LLC-PK1 cells.

Matsuoka M, Wispriyono B, Igisu H.

Department of Environmental Toxicology, University of Occupational

and Environmental Health, Kitakyyushu, Japan. masatomm@...

The c-fos, a member of the immediate early genes, has been reported

to be expressed in the renal proximal tubule in response to ischemic

and toxic injury. In the present study, effects of mercury chloride

(HgCl2) on the expression of c-fos were examined in LLC-PK1 cells.

The reverse transcription polymerase chain reaction (RT-PCR) analysis

for the semi-quantification of mRNA showed that the treatment of 20

microM HgCl2, markedly increased c-fos mRNA levels. The level of c-

fos mRNA began to increase after a 30-min exposure, peaked at 1 h and

then returned to the control level at 8 h. The HgCl2-induced c-fos

expression was abolished completely by actinomycin-D, indicating it

was due to transcriptional activation of the gene. Western blotting

immunodetection revealed accumulation of c-Fos protein after 1 h

exposure to 20 microM HgCl2. The cytotoxicity of HgCl2 as assayed by

mitochondrial dehydrogenase activity (MTT conversion) was observed

after 18 h exposure but not at 0.5-8 h. Also, the decrease in cell

viability was accompanied with DNA fragmentation, which is

characteristic of apoptosis. The present results showed that HgCl2

could induce the early expression of c-fos gene in a renal epithelial

cell line.

: Biomed Environ Sci. 2006 Feb;19(1):67-72. Links

Expression of c-fos in rat brain as a prelude marker of central

nervous system injury in response to methylmercury-stimulation.

Cheng JP, Wang WH, Jia JP, Zheng M, Shi W, Lin XY.

School of Environmental Science and Engineering, Shanghai Jiao Tong

University, Shanghai 200240, China. jpcheng@...

OBJECTIVE: To probe into the prelude marker of central nervous system

injury in response to methyl mercury chloride (MMC) stimulation and

the signal transduction molecular mechanism of injury in rat brain

induced by MMC. METHODS: The expression of c-fos mRNA in brain and

the expression of c-FOS protein in cortex, hippocampus and ependyma

were observed using reverse transcription polymerase chain reaction

(RT-PCR) and immunocytochemical methods. The control group was

injected with physiological saline of 0.9%, while the concentrations

for the exposure groups were 0.05 and 0.5, 5 mg/kg MMC respectively,

and the sampling times points were 20, 60, 240, 1440 min. RESULTS:

The expression of c-FOS protein in cortex and hippocampus increased

significantly, the accumulation of mercury in the brain induced by

0.05 mg/Kg MMC for 20 min had no significant difference compared with

the control group. The mean value was 0.0044 mg/Kg, while the protein

c-FOS expression had significant difference compared with the control

group (P < 0.01). More sensitive expression occurred in hippocampus

and cortex, but not in ependyma. Conclusion The expression of c-FOS

protein in cortex and hippocampus can predict the neurotoxicity of

MMC in the early time, and immediately early gene (IEG) c-fos

participates in the process of brain injury induced by MMC.

1: Toxicol Sci. 2000 Feb;53(2):361-8. Links

Mercury chloride activates c-Jun N-terminal kinase and induces c-jun

expression in LLC-PK1 cells.

Matsuoka M, Wispriyono B, Iryo Y, Igisu H.

Department of Environmental Toxicology, University of Occupational

and Environmental Health, Kitakyushu, Japan. masatomm@...

In response to various environmental stresses including heavy metals,

the c-Jun N-terminal kinase (JNK) is phosphorylated and then it

phosphorylates c-Jun protein. In the present study, effects of

mercury chloride (HgCl2) on JNK signalling pathway were examined in

LLC-PK1 cells. When exposed to 10 or 20 microM HgCl2, the level of

phosphorylated JNK and the activity of JNK assayed in vitro using

glutathione-S-transferase-c-Jun as substrate increased markedly. The

level of phosphorylated JNK increased 30 min after HgCl2 exposure and

remained elevated even at 8 h. On the other hand, no changes were

found in the total amount of JNK protein. Consistent with the

activation of JNK, c-Jun proteins phosphorylated on Ser63 and Ser73

were accumulated in cells exposed to HgCl2. Concomitantly, the levels

of c-jun mRNA and c-Jun protein were elevated. When compared to other

heavy metal compounds such as manganese chloride, zinc chloride,

cadmium chloride, and lead chloride, HgCl2 could phosphorylate JNK

more markedly. Neither intracellular Ca2+ nor sulfhydryl groups

appeared to play a major role in the activation of JNK by HgCl2

exposure in this porcine renal epithelial cell line.

1: Environ Health Perspect. 1979 Aug;31:59-66. Links

Chemical induction of nondisjunction in drosophila.

Ramel C, Magnusson J.

Tests for chemically induced nondisjunction and loss of the sex

chromosomes in Drosophila were performed. Of 31 compounds tested four

gave rise only to an increase of XO exceptions, indicating the

induction of chromosome loss. Six compounds, all known spindle

inhibitors (colchicine, organic mercury, lead, and tin compounds)

gave rise to an increase both of XXY and XO or of only XXY. The

effect by metalloorganic compounds of which methylmercury was studied

particularly closely, follows a peculiar pattern. In females with

structurally normal X chromosomes only an increase of XX gametes is

obtained, while with X chromosomes heterozygous for long inversions

only O gametes are increased. The data indicates that the effect of

the metal compounds occurs at first meiosis and that the process is

connected with a meiotic drive, giving rise to a preferential

segregation of the two X chromosomes to the functioning pole. The

increase only of O gametes with structurally heterozygous X

chromosomes can tentatively be explained by a loss due to crossing

over within the inversion. An increase of the effect of methyl

mercury was obtained where the normal pairing of the X chromosomes

was interfered with by means of autosomal inversions. Likewise a

synergistic increase of nondisjunction was obtained when a

temperature chock of 10 degrees C was applied together with treatment

with methylmercury. It is concluded that chemical induction of

nondisjunction can be studied in Drosophila, but the sensitivity of

the test is rather low and large amount of material is required

1: Sci Total Environ. 1986 Jan;48(1-2):81-94. Links

Sister chromatid exchange (SCE) in Greenlandic Eskimos. Dose-response

relationship between SCE and seal diet, smoking, and blood cadmium

and mercury concentrations.

Wulf HC, Kromann N, Kousgaard N, Hansen JC, Niebuhr E, Albøge K.

The mutagenicity of the chromosomes of the peripheral lymphocytes of

147 Greenlandic Eskimos living in the district of Angmagssalik,

Greenland, and in Denmark, was evaluated by means of the sister

chromatid exchange (SCE) test. Thirty cells from each person were

examined. The purpose of the investigation was to determine if there

was any relationship between mutagenic activity and diet, and hence

the elements selenium, cadmium, mercury and lead. The probands were

divided into three groups according to their intake of seal meat or

industrially prepared food: group 1, those eating seal at least six

times per week; group 2, two to five times per week; and group 3 once

each week or not at all. The statistical analysis was performed by

means of multiple linear regression analyses, with diet, living

district, sex, age, tobacco smoking, and blood lead and mercury

concentrations as variables. Forty-eight percent of the variation in

SCE could be explained by differences in diet, living district, age,

and tobacco consumption. Groups 1 and 2 had a 1.7 and 0.65 times

higher SCE/cell, respectively, than group 3. For every additional 10

years of age of the probands, the SCE/cell increased by 0.4, and for

every 10 g of tobacco smoked per day the SCE/cell was 0.7 higher

compared to non-smokers. When priority was given to blood Hg

concentration in the calculation, 16.3% of the total variation in

SCE/cell could be explained. An increase in the blood Hg

concentration of 10 micrograms l-1 corresponded to an increase of 0.3

SCE/cell. In 92 individuals blood Se and Cd concentrations were also

analysed. The variables, tobacco smoking, diet, living district and

Cd explained 53% of the total variation in SCE. Giving priority to

the blood Hg and Cd concentrations, explained 21.4% of the total

variation in SCE/cell. An increase of 10 micrograms l-1 in blood Cd

and Hg corresponded to an increase in SCE/cell of 0.7 and 0.2,

respectively. No influence on the SCE/cell could be attributed to the

blood Pb and Se concentrations. Evaluated by the SCE test, seal diet,

smoking, living district and blood Hg and Cd concentrations all

contribute to mutagenicity in Greenlandic Eskimos, with seal diet as

the most important of the factors examined.

1: Toxicol Lett. 1984 Jun;21(3):247-53. Links

Mercury-induced segregational errors of chromosomes in human

lymphocytes and in Indian muntjac cells.

Verschaeve L, Kirsch-Volders M, ne C.

Segregational errors of chromosomes were studied in human lymphocytes

and in Indian muntjac fibroblasts exposed to methylmercury chloride

(CH3HgCl) or mercury chloride (HgCl2). The cells were exposed to the

mercury compounds only during a limited period of the pre-DNA

synthetic stage of the cell cycle or from that stage up to mitosis.

In the lymphocytes we observed a clear increase of C-mitotic figures

for both mercury compounds and for both exposure times. Segregational

errors were, however, much more important after the shorter exposure

period. Muntjac fibroblasts appear to be more sensitive to the

mercury than are the lymphocytes so that their suitability for the

study of C-mitosis may be questionable. The muntjac cells may be an

important tool for the study of polyploidy induction

1: Environ Res. 1998 May;77(2):68-72. Links

Mercury levels along the food chain and risk for exposed populations.

Renzoni A, Zino F, Franchi E.

Dipartimento di Biologia Ambientale, Università di Siena, Via delle

Cerchia 3, Siena, 53100, Italy.

Mercury was not regarded as a pollutant of primary importance until

many deaths due to mercury poisoning occurred in the 1950s. More

recently, adverse health effects have been documented at relatively

low exposure levels, and monitoring data must now be interpreted in

this light. The Mediterranean basin has been studied in great detail

over the past 20 years because of the anomalous natural presence of

mercury. Marine animals of this basin have higher mercury body

burdens than the same (or similar) species in the Atlantic. The

mercury found in marine organisms is mainly in the form of methyl

mercury. Long-term and frequent intake of seafood with high mercury

levels by populations living in coastal fishing villages is

associated with a toxic risk, especially in pregnant women. High

blood and hair concentrations of mercury have repeatedly been found

in fishermen of Tyrrhenian coastal villages. In some cases these

concentrations have been associated with an increase in DNA damage in

blood cells. High mercury levels in hair and blood of people from a

fishing village of Madeira have also been found. This information

deserves renewed scrutiny with regard to preventive efforts needed.

Copyright 1998 Academic Press.

1: Mutat Res. 1999 Sep 30;445(2):225-39. Links

Chromosomal aberrations and sister-chromatid exchanges in Lithuanian

populations: effects of occupational and environmental exposures.

Lazutka JR, Lekevicius R, Dedonyte V, Maciuleviciute-Gervers L,

Mierauskiene J, Rudaitiene S, Slapsyte G.

Department of Botany and Genetics, Vilnius University, Lithuania.

juozas.lazutka@...

Cytogenetic analysis of chromosomal aberrations (CA) in 175,229 cells

from 1113 individuals, both unexposed and occupationally or

environmentally exposed to heavy metals (mercury and lead), organic

(styrene, formaldehyde, phenol and benzo(a)pyrene) and inorganic

(sulfur and nitrogen oxides, hydrogen and ammonium fluorides)

volatile substances and/or ionizing radiation was performed. In

addition, 11,250 cells from 225 individuals were scored for the

frequency of sister-chromatid exchanges (SCE). Increased frequencies

of CA were found in all occupationally exposed groups. A principal

difference between the exposure to heavy metals and organic

substances was found: increase in the CA frequency was dependent on

duration of exposure to mercury but not dependent on duration of

exposure to styrene, formaldehyde and phenol. A higher CA incidence

was found in lymphocytes of children living in the vicinity of a

plant manufacturing phosphate fertilizers. This indicates that

children are a sensitive study group for the assessment of

environmental exposure. However, the results of SCE analysis in these

children were inconclusive. Exposure to ionizing radiation was found

to cause chromosome breaks and chromatid exchanges in Chernobyl clean-

up workers and chromatid breaks, chromatid exchanges, dicentric

chromosomes and chromosome translocations in workers from the

Ignalina Nuclear Power Plant. The increased frequency of chromatid

exchanges in individuals exposed to ionizing radiation was quite

unexpected. This may be attributed to the action of some unrecognized

life-style or occupational factors, or to be a result of radiation-

induced genomic instability. Also an increased SCE frequency was

found in lymphocytes of Chernobyl clean-up workers.

1: J Epidemiol Community Health. 1986 Jun;40(2):181-5. Links

Methylmercury exposure and mortality in southern Japan: a close look

at causes of death.

Tamashiro H, Arakaki M, Futatsuka M, Lee ES.

This study examines mortality patterns by cause of death to

investigate the effect of exposure to methylmercury in a small area

of Minamata City (Kumamoto Prefecture, Japan), which has the highest

concentration of patients with Minamata disease. Standardised

mortality ratios (SMRs) are computed by cause of death for the study

area, using the age specific rates of the entire city as a standard.

The SMRs for liver cancer and chronic liver disease in the study area

are significantly higher than unity and are consistent with the

mortality patterns of registered Minamata disease patients. While an

excess mortality is observed for cerebral haemorrhage, mortality from

cerebral infarction and other cerebrovascular diseases is

considerably lower in the study area. The multiple risk factors of

liver related diseases and a possible explanation for the

cerebrovascular mortality patterns are discussed to suggest further

investigation.

1: Int Arch Occup Environ Health. 2007 Aug;80(8):679-88. Epub 2007

Mar 15. Links

Age standardized cancer mortality ratios in areas heavily exposed to

methyl mercury.

Yorifuji T, Tsuda T, Kawakami N.

Hygiene and Preventive Medicine, Okayama University Graduate School

of Medicine, Dentistry and Pharmaceutical Sciences, 2-5-1 Shikata-

cho, Okayama, 700-8558, Japan, yorichan@....

OBJECTIVE: Methyl-mercury (MeHg) was discharged from a chemical

factory in Minamata, and consequently spread throughout the Shiranui

Sea in Kumamoto, Japan. Although many studies have focused on MeHg-

induced neurological disorders, the association between MeHg and

malignant neoplasms has not been adequately investigated. Therefore,

we explored this association using the age standardized mortality

ratio (ASMR) in an ecologic study over a wide area allowing for a

long empirical induction period. METHODS: The subjects were residents

in areas around the Shiranui Sea. We divided these areas into

exposure groups 1 (Minamata and Ashikita regions) and 2 (Amakusa

region). Exposure group 1 was contaminated from the late 1930s, and

exposure group 2 was contaminated from the late 1950s. In addition,

exposure group 1 was contaminated more heavily than exposure group 2.

There were 92,525 and 152,541 residents in each group in 1960,

respectively. We analyzed the cancer ASMR in both exposure groups

using data from two reference populations (Japan and Kumamoto

prefecture) from 1961 to 1997. There were 94,301,494 and 1,856,192

people in each reference group in 1960, respectively. We abstracted

population and mortality data from the censuses and the vital

statistics of the prefecture and Japan. RESULTS: An increased

leukemia ASMR and a decreased gastric cancer ASMR were observed in

both exposure groups, while other ASMRs were around unity and less

precise. Furthermore, the leukemia ASMRs were elevated differently

between the two exposure groups: the leukemia ASMR was already

elevated early in the study period in exposure group 1 and increased

gradually in exposure group 2. CONCLUSIONS: While the negative

association between MeHg and gastric cancer might be explained by

salt intake, the positive association between MeHg and leukemia could

not be explained by potential confounders. Despite some limitations

mainly due to its ecologic design, this study indicates the necessity

of an individual-level study evaluating the association between MeHg

and leukemia in regions with exposure to MeHg.

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

Looking for a deal? Find great prices on flights and hotels with

FareChase.