Tylenol b12 folate Re: [cheautism] arsenic in autism (small study), in food

[Guest guest]

" Out of 10 patients, 6 had initial urine samples containing arsenic in

greater concentration than healthy controls.... Thiamine

tetrahydrofurfuryl disulfide appears to have a beneficial clinical

effect on some autistic children, since 8 of the 10 children improved

clinically. We obtained evidence of an association of this increasingly

occurring disease with presence of urinary SH-reactive metals, arsenic

in particular. " (1)

Straightforward overview of arsenic in food (2)

" Arsenic reduced expression of endothelial NOS (eNOS) and iNOS genes.

Acetaminophen up-regulated eNOS and iNOS expression and NO production in

Phase-I, but reversed these effects in Phase-II. Results reveal that

acetaminophen increased the risk of arsenic-mediated hepatic oxidative

damage. Withdrawal of acetaminophen administration also increased

susceptibility of liver to hepatotoxicity. " (3)

[Markers] " ....could be reduced with simultaneous administration either

with folic acid or a combination of folic acid + vitamin B_12 .

Significantly, similar supplementations were found effective in

increasing the urinary clearance of arsenic. Together, these results

indicate that folic acid and vitamin B_12 may be effective to reduce the

arsenic-induced damage at molecular target level. " (4)

" Earlier, we proposed that the ability of folic acid and vitamin B_12 to

preserve systemic and mitochondrial function after short-term exposure

to arsenic may prevent further progression to more permanent injury and

pathological changes leading to cell death. To elucidate its

mechanism... Additionally, results of hepatic cell DNA fragmentation,

arsenic load of blood, hepatic tissue and urine, and histological

observations, all strongly support that both these supplements have

efficacy in preventing apoptotic changes and cellular damage. As the

mechanisms of actions of both of these supplements are methylation

related, a combined application was more effective. Results further

reveal new molecular targets through which folic acid and vitamin B_12

separately or in combination work to alleviate one critical component of

arsenic-induced liver injury: mitochondria dysfunction. " (5)

//

>

> 1. Treatment of autism spectrum children with thiamine

> tetrahydrofurfuryl disulfide: a pilot study.

> <http://www.ncbi.nlm.nih.gov/pubmed/12195231>

> Lonsdale D, Shamberger RJ, Audhya T.

> Neuro Endocrinol Lett. 2002 Aug;23(4):303-8.

>

>

> 2. */Arsenic in foods - Mercola & Oz/*

>

>

http://articles.mercola.com/sites/articles/archive/2012/01/22/toxic-metals-on-fr\

uit-juices.aspx

>

3. Acetaminophen increases the risk of arsenic-mediated development of

hepatic damage in rats by enhancing redox-signaling mechanism.

<http://www.ncbi.nlm.nih.gov/pubmed/22120977>

Majhi CR, Khan S, Marcus Leo MD, Prawez S, Kumar A, Sankar P, Telang AG,

Sarkar SN.

Environ Toxicol. 2011 Nov 25. doi: 10.1002/tox.20785.

http://onlinelibrary.wiley.com/doi/10.1002/tox.20785/abstract

We evaluated whether the commonly used analgesic-antipyretic drug

acetaminophen can modify the arsenic-induced hepatic oxidative stress

and also whether withdrawal of acetaminophen administration during the

course of long-term arsenic exposure can increase susceptibility of

liver to arsenic toxicity. Acetaminophen was co-administered orally to

rats for 3 days following 28 days of arsenic pre-exposure (Phase-I) and

thereafter, acetaminophen was withdrawn, but arsenic exposure was

continued for another 28 days (Phase-II). Arsenic increased lipid

peroxidation and reactive oxygen species (ROS) generation, depleted

glutathione (GSH), and decreased superoxide dismutase (SOD), catalase,

glutathione peroxidase (GPx), and glutathione reductase (GR) activities.

Acetaminophen caused exacerbation of arsenic-mediated lipid peroxidation

and ROS generation and further enhancement of serum alanine

aminotransferase and aspartate aminotransferase activities. In Phase-I,

acetaminophen caused further GSH depletion and reduction in SOD,

catalase, GPx and GR activities, but in Phase-II, only GPx and GR

activities were more affected. Arsenic did not alter basal and inducible

nitric oxide synthase (iNOS)-mediated NO production, but decreased

constitutive NOS (cNOS)-mediated NO release. Arsenic reduced expression

of endothelial NOS (eNOS) and iNOS genes. Acetaminophen up-regulated

eNOS and iNOS expression and NO production in Phase-I, but reversed

these effects in Phase-II. Results reveal that acetaminophen increased

the risk of arsenic-mediated hepatic oxidative damage. Withdrawal of

acetaminophen administration also increased susceptibility of liver to

hepatotoxicity. Both ROS and NO appeared to mediate lipid peroxidation

in Phase-I, whereas only ROS appeared responsible for peroxidative

damage in Phase-II.

4. Folic acid or combination of folic acid and vitamin B_12 prevents

short-term arsenic trioxide-induced systemic and mitochondrial

dysfunction and DNA damage

<http://onlinelibrary.wiley.com/doi/10.1002/tox.20442/abstract>

Environmental Toxicology

Volume 24, Issue 4, August 2009, Pages: 377--387, Sangita Majumdar et al

5. Antiapoptotic efficacy of folic acid and vitamin B_12 against

arsenic-induced toxicity

<http://onlinelibrary.wiley.com/doi/10.1002/tox.20648/abstract>

Environmental Toxicology

Sangita Majumdar et al

Article first published online : 8 DEC 2010, DOI: 10.1002/tox.20648

Earlier, we proposed that the ability of folic acid and vitamin B_12 to

preserve systemic and mitochondrial function after short-term exposure

to arsenic may prevent further progression to more permanent injury and

pathological changes leading to cell death. To elucidate its mechanism,

the present study examined the antiapoptotic efficacy of folic acid and

vitamin B_12 against short-term arsenic exposure-induced hepatic

mitochondria oxidative stress and dysfunction. Sixteen to eighteen weeks

old male albino rats weighing 140--150 × g were divided into five

groups: Control (A), Arsenic-treated (, Arsenic + folic acid ©,

Arsenic +vitamin B_12 (D), and Arsenic + folic acid + vitamin B_12 (E).

Data generated indicated that folic acid and vitamin B_12 separately or

in combination can give significant protection against alterations in

oxidative stress and apoptotic marker parameters and downstream changes

in mitochondria, namely pro-oxidative (NO, TBARS, OH^- ) and

antioxidative defense (SOD, CAT, GSH) markers, iNOS protein expression,

mitochondrial swelling, cytochrome c oxidase and Ca^2+ -ATPase activity,

Ca^2+ content, caspase-3 activity. Additionally, results of hepatic cell

DNA fragmentation, arsenic load of blood, hepatic tissue and urine, and

histological observations, all strongly support that both these

supplements have efficacy in preventing apoptotic changes and cellular

damage. As the mechanisms of actions of both of these supplements are

methylation related, a combined application was more effective. Results

further reveal new molecular targets through which folic acid and

vitamin B_12 separately or in combination work to alleviate one critical

component of arsenic-induced liver injury: mitochondria dysfunction.