Wrong on thimerosal-Globe and Mail

[Guest guest]

Can anyone access this entire article?

Here is a slide presentation from Dr. Gold.

http://tinyurl.com/avmlo

http://tinyurl.com/dhxwe

By RONALD GOLD

Thursday, July 7, 2005 Page A14Key

MD

Toronto -- Usually I read Mallick's rational columns with

great pleasure. Unfortunately, her column Boycotting Is My New Drug Of

Choice (July 2) repeats the nonsense spouted by Kennedy Jr.

about the totally unsubstantiated risks of thimerosal in vaccines.

While I am fully aware of the increasing dangers of Big Pharma,

especially in relation to vaccine supply (the world is now dependent

on a handful of producers), I also know that there is no valid

scientific evidence whatsoever to support the myth that thimerosal in

vaccines causes autism or any form of brain damage.

Repeating Mr. Kennedy's inaccurate statements will do great harm.

[Guest guest]

> By RONALD GOLD

>

> Thursday, July 7, 2005 Page A14Key

>

> MD

>

> Toronto -- Usually I read Mallick's rational columns with

> great pleasure. Unfortunately, her column Boycotting Is My New Drug

Of

> Choice (July 2) repeats the nonsense spouted by Kennedy Jr.

> about the totally unsubstantiated risks of thimerosal in vaccines.

>

> While I am fully aware of the increasing dangers of Big Pharma,

> especially in relation to vaccine supply (the world is now dependent

> on a handful of producers), I also know that there is no valid

> scientific evidence whatsoever to support the myth that thimerosal

in

> vaccines causes autism or any form of brain damage.

>

> Repeating Mr. Kennedy's inaccurate statements will do great harm.

Yeah, thimerosal can only cause damage if it is not in vaccines, but

when you put it in vaccines and inject it into infants, it magically

becomes safe. The thimerosal fairy makes all that possible...

Neurotoxicology. 2005 Jun;26(3):407-16. Related Articles, Links

Mitochondrial Mediated Thimerosal-Induced Apoptosis in a Human

Neuroblastoma Cell Line (SK-N-SH).

Humphrey ML, Cole MP, Pendergrass JC, Kiningham KK.

Department of Pharmacology, Joan C. School of Medicine,

Marshall University, 1542 Spring Valley Drive, Huntington, WV 25704-

9388, USA.

Environmental exposure to mercurials continues to be a public health

issue due to their deleterious effects on immune, renal and

neurological function. Recently the safety of thimerosal, an ethyl

mercury-containing preservative used in vaccines, has been questioned

due to exposure of infants during immunization. Mercurials have been

reported to cause apoptosis in cultured neurons; however, the

signaling pathways resulting in cell death have not been well

characterized. Therefore, the objective of this study was to identify

the mode of cell death in an in vitro model of thimerosal-induced

neurotoxicity, and more specifically, to elucidate signaling pathways

which might serve as pharmacological targets. Within 2h of thimerosal

exposure (5muM) to the human neuroblastoma cell line, SK-N-SH,

morphological changes, including membrane alterations and cell

shrinkage, were observed. Cell viability, assessed by measurement of

lactate dehydrogenase (LDH) activity in the medium, as well as the 3-

[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT)

assay, showed a time- and concentration-dependent decrease in cell

survival upon thimerosal exposure. In cells treated for 24h with

thimerosal, fluorescence microscopy indicated cells undergoing both

apoptosis and oncosis/necrosis. To identify the apoptotic pathway

associated with thimerosal-mediated cell death, we first evaluated

the mitochondrial cascade, as both inorganic and organic mercurials

have been reported to accumulate in the organelle. Cytochrome c was

shown to leak from the mitochondria, followed by caspase 9 cleavage

within 8h of treatment. In addition, poly(ADP-ribose) polymerase

(PARP) was cleaved to form a 85kDa fragment following maximal caspase

3 activation at 24h. Taken together these findings suggest

deleterious effects on the cytoarchitecture by thimerosal and

initiation of mitochondrial-mediated apoptosis.

PMID: 15869795 [PubMed - in process]