Re: Low glutathione

November 5, 2003

Malisa,

IV NAC is probably a good way to increase glutathione. I think there

are a few kids on the list who get IV NAC (I think Anne's sons do). I

am not sure which lab offers the best methodology for glutathione

testing, but we have used Spectra-Cell twice. There probably is

another lab that the mito experts prefer to use. My son is doing much

better since we started treating his low glutathione. One study

reports that Parkinson's patients (who are thought to have Complex I

disorders) showed a 42% decline in disability after 30 days of daily

infusions.

I choose their new Profile 4000 which included thiamine, riboflavin,

niacinamide, vitamin B6, folate, pantothenate, biotin, carnitine,

vitamin D, calcium, zinc, magnesium, glutathione, CoQ-10, selenium,

vitamin E, Alpha Lipoic acid, total anti-oxidant function, and

lymphocyte proliferation index all for about $225 (this is the

pre-paid price and his doctor didn't charge anything to draw labs).

Our insurance covered the testing at 100% and Spectra-cell credited my

credit card when the insurance paid.

They also offer other profiles that include cysteine, glucose-insulin

interaction and fructose intolerance among other things.

You can get more info from their website--

http://www.spectracell.com/assessing-nutrient.html

I did notice that none of the new Profiles are listed. I think that

they have added two new profiles--the Profile 4000 and Profile 5000.

Prog Neuropsychopharmacol Biol Psychiatry. 1996

Oct;20(7):1159-70.

Links

Reduced intravenous glutathione in the treatment of

early Parkinson's disease.

Sechi G, Deledda MG, Bua G, Satta WM, Deiana GA, Pes GM, ti G.

Department of Neurology, University of Sassari, Italy.

1.

Several studies have demonstrated a deficiency in reduced glutathione

(GSH) in the nigra of patients with Parkinson's Disease (PD). In

particular, the magnitude of reduction in GSH seems to parallel the

severity of the disease. This finding may indicate a means by which the

nigra cells could be therapeutically supported. 2. The authors studied

the effects of GSH in nine patients with early, untreated PD. GSH was

administered intravenous, 600 mg twice daily, for 30 days, in an open

label fashion. Then, the drug was discontinued and a follow-up

examination carried-out at 1-month interval for 2-4 months. Thereafter,

the patients were treated with carbidopa-levodopa. 3. The clinical

disability was assessed by using two different rating scale and the

Webster Step-Second Test at baseline and at 1-month interval for 4-6

months. All patients improved significantly after GSH therapy, with a

42% decline in disability. Once GSH was stopped the therapeutic effect

lasted for 2-4 months. 4. Our data indicate that in untreated PD

patients GSH has symptomatic efficacy and possibly retards the

progression of the disease.

Med Hypotheses. 2001 Apr;56(4):472-7.

Links

Therapeutic potential of N-acetylcysteine in

age-related mitochondrial neurodegenerative diseases.

Banaclocha MM.

Department of Pathology, Hospital La Paz, Madrid, Spain.

marbanaci@...

Increasing

lines of evidence suggest a key role for mitochondrial damage in

neurodegenerative diseases. Brain aging, Parkinson's disease,

Alzheimer's disease, Huntington's disease and Friedreich's ataxia have

been associated with several mitochondrial alterations including

impaired oxidative phosphorylation. Mitochondrial impairment can

decrease cellular bioenergetic capacity, which will then increase the

generation of reactive oxygen species resulting in oxidative damage and

programmed cell death. This paper reviews the mechanisms of

N-acetylcysteine action at the cellular level, and the possible

usefulness of this antioxidant for the treatment of age-associated

neurodegenerative diseases. First, this thiol can act as a precursor

for glutathione synthesis as well as a stimulator of the cytosolic

enzymes involved in glutathione regeneration. Second, N-acetylcysteine

can act by direct reaction between its reducing thiol group and

reactive oxygen species. Third, it has been shown that N-acetylcysteine

can prevent programmed cell death in cultured neuronal cells. And

finally, N-acetylcysteine also increases mitochondrial complex I and IV

specific activities both in vitro and in vivo in synaptic mitochondrial

preparations from aged mice. In view of the above, and because of the

ease of its administration and lack of toxicity in humans, the

potential usefulness of N-acetylcysteine in the treatment of

age-associated mitochondrial neurodegenerative diseases deserves

Biochem Pharmacol. 2002 Sep;64(5-6):1037-48.

Links

Glutathione, iron and Parkinson's disease.

Bharath S, Hsu M, Kaur D, Rajagopalan S, Andersen JK.

Buck Institute For Age Research, 8001 Redwood Boulevard, Novato, CA

94945, USA.

Parkinson's

disease (PD) is a progressive neurodegenerative disease involving

neurodegeneration of dopaminergic neurons of the substantia nigra (SN),

a part of the midbrain. Oxidative stress has been implicated to play a

major role in the neuronal cell death associated with PD. Importantly,

there is a drastic depletion in cytoplasmic levels of the thiol

tripeptide glutathione within the SN of PD patients. Glutathione (GSH)

exhibits several functions in the brain chiefly acting as an

antioxidant and a redox regulator. GSH depletion has been shown to

affect mitochondrial function probably via selective inhibition of

mitochondrial complex I activity. An important biochemical feature of

neurodegeneration during PD is the presence of abnormal protein

aggregates present as intracytoplasmic inclusions called Lewy bodies.

Oxidative damage via GSH depletion might also accelerate the build-up

of defective proteins leading to cell death of SN dopaminergic neurons

by impairing the ubiquitin-proteasome pathway of protein degradation.

Replenishment of normal glutathione levels within the brain may hold an

important key to therapeutics for PD. Several reports have suggested

that iron accumulation in the SN patients might also contribute to

oxidative stress during PD.

Free Radic Res. 2002 Apr;36(4):421-7.

Links

Coenzyme Q cytoprotective mechanisms for

mitochondrial complex I cytopathies involves NAD(P)H: quinone

oxidoreductase 1(NQO1).

Chan TS, Teng S, JX, Galati G, Khan S, O'Brien PJ.

Faculty of Pharmacy, University of Toronto, Ont, Canada.

The

commonest mitochondrial diseases are probably those impairing the

function of complex I of the respiratory electron transport chain. Such

complex I impairment may contribute to various neurodegenerative

disorders e.g. Parkinson's disease. In the following, using hepatocytes

as a model cell, we have shown for the first time that the cytotoxicity

caused by complex I inhibition by rotenone but not that caused by

complex III inhibition by antimycin can be prevented by coenzyme Q

(CoQ1) or menadione. Furthermore, complex I inhibitor cytotoxicity was

associated with the collapse of the mitochondrial membrane potential

and reactive oxygen species (ROS) formation. ROS scavengers or

inhibitors of the mitochondrial permeability transition prevented

cytotoxicity. The CoQ1 cytoprotective mechanism required CoQ1 reduction

by DT-diaphorase (NQO1). Furthermore, the mitochondrial membrane

potential and ATP levels were restored at low CoQ1 concentrations (5

microM). This suggests that the CoQ1H2 formed by NQO1 reduced complex

III and acted as an electron bypass of the rotenone block. However

cytoprotection still occurred at higher CoQ1 concentrations (>10

microM), which were less effective at restoring ATP levels but readily

restored the cellular cytosolic redox potential (i.e. lactate: pyruvate

ratio) and prevented ROS formation. This suggests that CoQ1 or

menadione cytoprotection also involves the NQO1 catalysed reoxidation

of NADH that accumulates as a result of complex I inhibition. The

CoQ1H2 formed would then also act as a ROS scavenger.

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