FW: [abmd] Glutathione deficiency leads to mitochondrial damage in brain

August 8, 2007

-----Original Message-----

From: abmd [mailto:abmd ] On Behalf Of

Binstock

Sent: Wednesday, August 08, 2007 7:59 PM

Implication: Giving Tylenol increases the likelihood of brain damage in

children already low in GSH.

- - - - whole text free online

http://www.pubmedce

<http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=51136 & blobtype=pdf>

ntral.nih.gov/picrender.fcgi?artid=51136 & blobtype=pdf

Proc Natl Acad Sci U S A. 1991 March 1; 88(5): 1913–1917.

Glutathione deficiency leads to mitochondrial damage in brain.

A Jain, J Mårtensson, E Stole, P A Auld, and A Meister

Department of Pediatrics, Cornell University Medical College, New York, NY

10021.

Glutathione deficiency induced in newborn rats by giving buthionine

sulfoximine, a selective inhibitor of gamma-glutamylcysteine synthetase,

led to markedly decreased cerebral cortex glutathione levels and striking

enlargement and degeneration of the mitochondria . These effects were

prevented by giving glutathione monoethyl ester , which relieved the

glutathione deficiency, but such effects were not prevented by giving

glutathione, indicating that glutathione is not appreciably taken up by

the cerebral cortex . Some of the oxygen used by mitochondria is known to

be converted to hydrogen peroxide. We suggest that in glutathione

deficiency, hydrogen peroxide accumulates and damages mitochondria .

Glutathione, thus, has an essential function in mitochondria under normal

physiological conditions . Observations on turnover and utilization of

brain glutathione in newborn, preweaning, and adult rats show that (i)

some glutathione turns over rapidly (t 1/2, approximately 30 min in

adults, approximately 8 min in newborns), (ii) several pools of

glutathione probably exist, and (iii) brain utilizes plasma glutathione,

probably by gamma-glutamyl transpeptidase-initiated pathways that account

for some, but not all, of the turnover; thus, there is recovery or

transport of cysteine moieties. These studies provide an animal model for

the human diseases involving glutathione deficiency and are relevant to

oxidative phenomena that occur in the newborn.

August 9, 2007

Thanks Nagla for always sharing what you can in regards to anything

pertaining to the alternative Bio-med route and of course on any

research study going on.

I never thought I would have to learn so much & wear many hats, become

a " jack of all trades " for my son, but these past years on what I know

now in regards to this mission here. I am grateful. It helps to keep

the network going and can relate with others who respect anyone else's

opinion or belief when seeking other avenues.

Thanks,

Irma

>

> -----Original Message-----

> From: abmd [mailto:abmd ] On Behalf

Of

> Binstock

> Sent: Wednesday, August 08, 2007 7:59 PM

>

> Implication: Giving Tylenol increases the likelihood of brain damage in

> children already low in GSH.

>

> - - - - whole text free online

> http://www.pubmedce

>

<http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=51136 & blobtype=pdf>

> ntral.nih.gov/picrender.fcgi?artid=51136 & blobtype=pdf

>

> Proc Natl Acad Sci U S A. 1991 March 1; 88(5): 1913ï¿½1917.

>

> Glutathione deficiency leads to mitochondrial damage in brain.

>

> A Jain, J Mï¿½rtensson, E Stole, P A Auld, and A Meister

> Department of Pediatrics, Cornell University Medical College, New

York, NY

> 10021.

>

> Glutathione deficiency induced in newborn rats by giving buthionine

> sulfoximine, a selective inhibitor of gamma-glutamylcysteine synthetase,

> led to markedly decreased cerebral cortex glutathione levels and

striking

> enlargement and degeneration of the mitochondria . These effects were

> prevented by giving glutathione monoethyl ester , which relieved the

> glutathione deficiency, but such effects were not prevented by giving

> glutathione, indicating that glutathione is not appreciably taken up by

> the cerebral cortex . Some of the oxygen used by mitochondria is

known to

> be converted to hydrogen peroxide. We suggest that in glutathione

> deficiency, hydrogen peroxide accumulates and damages mitochondria .

> Glutathione, thus, has an essential function in mitochondria under

normal

> physiological conditions . Observations on turnover and utilization of

> brain glutathione in newborn, preweaning, and adult rats show that (i)

> some glutathione turns over rapidly (t 1/2, approximately 30 min in

> adults, approximately 8 min in newborns), (ii) several pools of

> glutathione probably exist, and (iii) brain utilizes plasma glutathione,

> probably by gamma-glutamyl transpeptidase-initiated pathways that

account

> for some, but not all, of the turnover; thus, there is recovery or

> transport of cysteine moieties. These studies provide an animal

model for

> the human diseases involving glutathione deficiency and are relevant to

> oxidative phenomena that occur in the newborn.

>

August 9, 2007

Thanks Nagla for always sharing what you can in regards to anything

pertaining to the alternative Bio-med route and of course on any

research study going on.

I never thought I would have to learn so much & wear many hats, become

a " jack of all trades " for my son, but these past years on what I know

now in regards to this mission here. I am grateful. It helps to keep

the network going and can relate with others who respect anyone else's

opinion or belief when seeking other avenues.

Thanks,

Irma

>

> -----Original Message-----

> From: abmd [mailto:abmd ] On Behalf

Of

> Binstock

> Sent: Wednesday, August 08, 2007 7:59 PM

>

> Implication: Giving Tylenol increases the likelihood of brain damage in

> children already low in GSH.

>

> - - - - whole text free online

> http://www.pubmedce

>

<http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=51136 & blobtype=pdf>

> ntral.nih.gov/picrender.fcgi?artid=51136 & blobtype=pdf

>

> Proc Natl Acad Sci U S A. 1991 March 1; 88(5): 1913ï¿½1917.

>

> Glutathione deficiency leads to mitochondrial damage in brain.

>

> A Jain, J Mï¿½rtensson, E Stole, P A Auld, and A Meister

> Department of Pediatrics, Cornell University Medical College, New

York, NY

> 10021.

>

> Glutathione deficiency induced in newborn rats by giving buthionine

> sulfoximine, a selective inhibitor of gamma-glutamylcysteine synthetase,

> led to markedly decreased cerebral cortex glutathione levels and

striking

> enlargement and degeneration of the mitochondria . These effects were

> prevented by giving glutathione monoethyl ester , which relieved the

> glutathione deficiency, but such effects were not prevented by giving

> glutathione, indicating that glutathione is not appreciably taken up by

> the cerebral cortex . Some of the oxygen used by mitochondria is

known to

> be converted to hydrogen peroxide. We suggest that in glutathione

> deficiency, hydrogen peroxide accumulates and damages mitochondria .

> Glutathione, thus, has an essential function in mitochondria under

normal

> physiological conditions . Observations on turnover and utilization of

> brain glutathione in newborn, preweaning, and adult rats show that (i)

> some glutathione turns over rapidly (t 1/2, approximately 30 min in

> adults, approximately 8 min in newborns), (ii) several pools of

> glutathione probably exist, and (iii) brain utilizes plasma glutathione,

> probably by gamma-glutamyl transpeptidase-initiated pathways that

account

> for some, but not all, of the turnover; thus, there is recovery or

> transport of cysteine moieties. These studies provide an animal

model for

> the human diseases involving glutathione deficiency and are relevant to

> oxidative phenomena that occur in the newborn.

>

August 9, 2007

Nagla,

If glutithione deficiency effects the mitochondria would that not make a

child hypo-active as opposed to hyperactive? If so, why would my child

be so extremely hyper? Oddly enough HBOT and Ozone seem to have helped

greatly with hyperactivity or does that have something to do with the

oxygen in the cells?Additionally said child also has what appears to be

hypotonia even with the activity level and is very pale even when iron

levels are normal, he doesn't tan much at all but has freckles on his

face almost the appearance of very low melanin everywhere else? I hope

your cellular biology is much better than mine the article you sent out

made my head spin can you clarify? One day I hope to see all medical and

science publications in cliff note form...grins....Trina

>

> Thanks Nagla for always sharing what you can in regards to anything

> pertaining to the alternative Bio-med route and of course on any

> research study going on.

> I never thought I would have to learn so much & wear many hats, become

> a " jack of all trades " for my son, but these past years on what I know

> now in regards to this mission here. I am grateful. It helps to keep

> the network going and can relate with others who respect anyone else's

> opinion or belief when seeking other avenues.

>

> Thanks,

> Irma

>

> >

> > -----Original Message-----

> > From: abmd <mailto:abmd%40yahoogroups.com>

> [mailto:abmd <mailto:abmd%40yahoogroups.com>] On Behalf

> Of

> > Binstock

> > Sent: Wednesday, August 08, 2007 7:59 PM

> >

> > Implication: Giving Tylenol increases the likelihood of brain damage in

> > children already low in GSH.

> >

> > - - - - whole text free online

> > http://www.pubmedce

> >

> <http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=51136 & blobtype=pdf

> <http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=51136 & blobtype=pdf>>

> > ntral.nih.gov/picrender.fcgi?artid=51136 & blobtype=pdf

> >

> > Proc Natl Acad Sci U S A. 1991 March 1; 88(5): 1913ï¿½1917.

> >

> > Glutathione deficiency leads to mitochondrial damage in brain.

> >

> > A Jain, J Mï¿½rtensson, E Stole, P A Auld, and A Meister

> > Department of Pediatrics, Cornell University Medical College, New

> York, NY

> > 10021.

> >

> > Glutathione deficiency induced in newborn rats by giving buthionine

> > sulfoximine, a selective inhibitor of gamma-glutamylcysteine synthetase,

> > led to markedly decreased cerebral cortex glutathione levels and

> striking

> > enlargement and degeneration of the mitochondria . These effects were

> > prevented by giving glutathione monoethyl ester , which relieved the

> > glutathione deficiency, but such effects were not prevented by giving

> > glutathione, indicating that glutathione is not appreciably taken up by

> > the cerebral cortex . Some of the oxygen used by mitochondria is

> known to

> > be converted to hydrogen peroxide. We suggest that in glutathione

> > deficiency, hydrogen peroxide accumulates and damages mitochondria .

> > Glutathione, thus, has an essential function in mitochondria under

> normal

> > physiological conditions . Observations on turnover and utilization of

> > brain glutathione in newborn, preweaning, and adult rats show that (i)

> > some glutathione turns over rapidly (t 1/2, approximately 30 min in

> > adults, approximately 8 min in newborns), (ii) several pools of

> > glutathione probably exist, and (iii) brain utilizes plasma glutathione,

> > probably by gamma-glutamyl transpeptidase-initiated pathways that

> account

> > for some, but not all, of the turnover; thus, there is recovery or

> > transport of cysteine moieties. These studies provide an animal

> model for

> > the human diseases involving glutathione deficiency and are relevant to

> > oxidative phenomena that occur in the newborn.

> >

August 9, 2007