Re: glutathione

[Guest guest]

In a message dated 7/10/02 1:52:14 PM Pacific Daylight Time, aplant@...

writes:

<< Evan's cystine was 27 (rr 45-77), his arginine was 176 (rr 23-86), and

his aspartic acid was 17. What was 's taurine (it is another

sulfur amino acid)?

>>

's taurine was normal at 87 (normal 0-240). So, now I'm confused...how

can he have a cystine of 1 (normal 36-58), but a normal taurine, if they're

both in the same sulfur amino acid cycle?

Dena (who gets VERY frustrated that her brain is fuzzy and cannot sort

through some of this biochemical stuff like it used to!!!)

[Guest guest]

In a message dated 7/10/02 1:52:14 PM Pacific Daylight Time, aplant@...

writes:

<< Evan had another glutathione infusion today. When they weighed him, I

was shocked. He has gained 3.6 pounds since starting the cornstarch

after the conference. Now he has gained a total of 7 pounds since

mid-March when he started IV glutathione. He has always struggled to

gain weight in the past. >>

That's great news! Since has been on the high complex carb diet, he

has gained almost 15 pounds since December! He still looks very thin because

of the proximal muscle wasting, but he's up to 79# (almost 5 foot tall)!

Dena

[Guest guest]

Deb,

Glutathione is not related to glutamate & glumatic acid. Glutamic

acid is an amino acid that can be excitotoxic and high levels of

may influence disease progression. Glutathione is a thiol antioxidant.

It protects you from oxidative stress. A deficiency of glutathione

can cause mitochondrial damage due to high levels of oxidative stress.

So glutathione is not directly related to glutamate, but higher levels

of glutathione could be protective against the oxidative stress that comes

from high levels of glutamate or glutamic acid.

In one Parkinson's study they showed that glutamate induces oxidative

stress and melatonin prevented the oxidant effect of glutamate.

Some info on CSF glutamine levels----

The normal concentration of most CSF amino acids is about 10% of the

corresponding plasma concentration. Reference intervals for premature infants

are not available. Please note that CSF should not be incubated or

allowed to stand at room temperature prior to being assayed for amino acids.

Glutamine is not stable in non- frozen samples.

Reference Interval:

Glycine, CSF: 0-20 µmol/L

Glutamic Acid, CSF: 0-10 µmol/L

Glutamine, CSF:

0-2 wks: 460-870 µmol/L

3 wks-6 mos: 400-780 µmol/L

7 mos-12 mos: 340-630 µmol/L

13 mos-30 mos: 240-600 µmol/L

31 mos-adult: 150-550 µmol/L

I hope this helps,

J Pineal Res 2001 Nov;31(4):356-62

Glutamate induces oxidative stress not mediated by glutamate receptors

or cystine transporters: protective effect of melatonin and other antioxidants.

Herrera F, Sainz RM, Mayo JC, V, Antolin I, C.

Departamento de Morfologia y Biologia Celular, Facultad de Medicina,

n Claveria s/n, 33006 Oviedo, Spain.

Glutamate is responsible for most of the excitatory synaptic activity

and oxidative stress induction in the mammalian brain. This amino acid

is increased in the substantia nigra in parkinsonism due to the lack of

dopamine restraint to the subthalamic nucleus. Parkinson's disease also

shows an increase of iron levels in the substantia nigra and a decrease

of glutathione, the antioxidant responsible for the ascorbate radical recycling.

Considered together, these facts could make the antioxidant ascorbate behave

as a pro-oxidant in parkinsonism. Since both glutamate and ascorbate are

present in the synaptosomes and neurons of substantia nigra, we tested

1) if glutamate is able to induce oxidative stress independently of its

excitatory activity, and 2) if ascorbate may have synergistic effects with

glutamate when these two molecules co-exist. Brains were homogenized in

order to disrupt membranes and render membrane receptors and intracellular

signaling pathways non-functional. In these homogenates glutamate induced

lipid peroxidation, indicating that this amino acid also may cause oxidative

stress not mediated by its binding to glutamate receptors or cystine transporters.

Ascorbate also induced lipid peroxidation thus behaving as a pro-oxidant.

Both substances together produced an additive effect but they did not synergize.

Given that melatonin is a potent physiological antioxidant with protective

effects in models of neurotoxicity, we tested the

role of this secretory product on the pro-oxidant effect of both

compounds given separately or in combination. We also checked the protective

ability of several other antioxidants. Pharmacological doses of melatonin

(millimolar), estrogens, pinoline and trolox (micromolar) prevented the

oxidant effect of glutamate, ascorbate, and the combination of both substances.

Potential therapeutic application of these results is discussed.

VisibleWorship@... wrote:

all of andrew's tests...if there is

a gluta-anything...it is elevated...I wondered what this means and am going

to ask Korson but I will give you a stab at it...one test says "of note,

glutamic acid is not elevated to the extent seen in glutamic acid decarboxylase

deficiency" but the othere tests where the gluta-whatever is elevated

she doesn't say anything, so I wondered if it was really close and all...on

this particular test...

CSF Amino Acid Test...his glutamic

acid is 11.3 with the NL's (0.0-3.8)...anyone got a clue about this?

sorry i am late in responding to these

posts but I have had a throat infection (icky) and have been in bed since

Monday night...

thanks

deb

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