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Nebulized glutathione: an inexpensive form and the relationship to sulfite oxidase enzyme and high urine sulfite.

The original publication on the benefit of nebulized glutathione (GSH) for emphysema and chronic obstructive pulmonary disease (COPD) employed a solution of GSH prepared by a compounding pharmacy, first published at 60 mg/ml and later used at 100 mg/ml. (1) Later, nebulized GSH was found helpful in some cases of asthma. (2) It has been of some assistance with Parkinson's disease, but the intravenous route is superior. (3) Now there is a much less expensive method of utilizing nebulized GSH.

The inexpensive version of nebulized GSH uses the same plastic nebulizer and air pump as previously, but with an over-the-counter GSH supplement. L-Glutathione Plus by Theranaturals Inc. (866-435-6599) combines 200 mg of reduced GSH with 55 mg of sodium bicarbonate per capsule. The contents of one capsule placed in 1 teaspoon (~5 ml) of water or saline in a nebulizer will foam slightly as the sodium salt of GSH is produced. This furnishes 200 mg of GSH in a dilution that is friendlier to the respiratory tract mucosa than solutions of 100 or especially 200 mg per ml.

For any pulmonary difficulty wherein GSH is to be so employed, it is advisable to check for elevation of urinary sulfite. Sulfite is an all-over sensitizing factor because of its oxidative potential. 3% to 10% of asthmatics are sensitive to sulfite, with intensification of asthmatic reaction with added sulfur compounds or sulfite, and demonstrate elevated levels of urine sulfite. (4) Some COPD patients demonstrate similarly.

Sulfur is one of the essential nutrients of which, with a reasonable amount of food intake, there is more than required. The "getting rid of extra sulfur system" proceeds in two steps. First, there is conversion to sulfite, followed by rapid conversion of sulfite to harmless sulfate by the enzyme sulfite oxidase.5 The function of sulfite oxidase seems the limiting difficulty in cases of elevated urine sulfite.

Sulfite oxidase has cofactors of molybdenum, pyridoxine, cobalamine, and other influences. In the clinic where the writer practices, for some years, molybdenum was thought to be the limiting cofactor. Numerous cases of elevated urine sulfite resolved after supplying well-absorbed molybdenum by mouth or by the intravenous route if absorption was compromised.

In some, another difficulty arises. In one patient, urine sulfite registered at 40 mg/L by sulfite dipstick. (6) There was no lowering of sulfite level with molybdenum by oral, intravenous, or continued intramuscular injection. The patient was self-administering a daily oral B-vitamin multiple and 1000 mcg cyanocobalamin weekly by intramuscular injection. The addition of pyridoxal-5'-phosphate (P5 P; 50 mg daily) reduced urine sulfite to zero within one day. Without further evaluation, it was presumed that this person did not efficiently convert pyridoxine to the active vitamin B6 form, P5P.

If this surmise is true, it would illustrate that not all sulfite oxidase deficiency is the result of a fatal genetic mutation, as published. (7-10) Failure to absorb or activate cofactors could result in limited sulfite oxidase activity and leave a substantial amount of sulfite with a degree of the deleterious effects described.

Further, it has been demonstrated that heavy metal ions can disrupt function of sulfite oxidase. (11) This could mean that elevated urine sulfite in some instances might be an indication of a toxic burden of heavy metals. The converse was not demonstrated in the clinic. Most cases of heavy metal burden did not show elevated urine sulfite. However, because of the sulfur compound included in intravenous chelation therapy, all patients are checked for urine sulfite before chelation. Elevated levels of sulfite are reduced before application of chelation.


(1.) Lamson DW, Brignall MS. The use of nebulized glutathione in the treatment of emphysema: a case report. Ahem Med Rev. 2000;5(4):429-431.

(2.) Private communication from James Seymour, RPh; Key Compounding Pharmacy; Federal Way, Washington. 800878-1322.

(3.) Hauser RA, Lyons KE, McClain T, Carter 5, Perlmutter D. Randomized, double blind, pilot evaluation of intravenous glutathione in Parkinson's disease. Mov Disord. 2009;24(7):979-983.

(4.) Vally H, Misso NL, Madan V. Clinical effects of sulphite additives. Clin Exp Allergy. 2009;39(11):1643-1651.

(5.) Qiu JA, Wilson HL, Rajagopalan KV. Structure-based alteration of substrate specificity and catalytic activity of sulfite oxidase from sulfite oxidation to nitrate reduction. Biochemistry. 2012;51(61):1134-1147.

(6.) Quantofix Sulfite; 91306.

(7.) Sass JO, Gunduz A, Araujo Rodrigues Funayama C, et al. Functional deficiencies of sulfite oxidase: Differential diagnoses in neonates presenting with intractable seizures and cystic encephalomalacia. Brain Dev. 2010 Aug;32(7):544-549.

(8.) Tan WH, Eichler FS, Hoda 5, et al. Isolated sulfite oxidase deficiency; a case report with a novel mutation and review of the literature. Pediatrics. 2005;116(3):757-766.

(9.) Karakas E, Kisker C. Structural analysis of missense mutations causing isolated sulfite oxidase deficiency. Dalton Trans. 2005;(21 ):3459-3463,

(10.) Hobson EE, Thomas S, Crofton PM, Murray AD, Dean IC, Lloyd D. Isolated sulphite oxidase deficiency mimics the features of hypoxic ischaemic encephalopathy. Eur J Pediatr. 2005;164(11):655-659.

(11.) Neumann M, Leimkuhler S. Heavy metal ions inhibit molybdoenzyme activity by binding to the dithiolene moiety of molybdopterin in Escherichia coli. FEBS I. 2008;275(22):5678-5689.

by Davis W. Lamson, MS, ND

Tahoma Clinic, Renton, Washington;
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Author:Lamson, Davis W.
Publication:Townsend Letter
Geographic Code:1USA
Date:Dec 1, 2013
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