Suggested Mechanisms of Action of Vitamin B-17

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Suggested Mechanisms of Action of Vitamin B-17

 

Charles Gurchot, Ph.D.

Oral doses of Vitamin B-17 seem not to much affected by the action

of the acid medium of the stomach, but pass into the intestine where

the substance is acted upon by bacterial enzymes.

 

In the intestine the enzyme complex Emulsin containing the enzymes

Beta-glucosidase, Benzocyanase, and others, degrades the Amygdalin

into four components: Hydrocyanic acid, Benzaldehyde, Prunasin, and

Mandelonitrile, which are absorbed into the lymph and portal

circulations.

 

Cyanide is converted to thiocyanate probably in the blood

circulation, and certainly in the liver by the enzyme rhodanese in

the presence of sulfur-bearing compounds.1,2 The circulating

thiocyanate exerts certain physiological effects on blood pressure

and thyroid action, and is not excreted rapidly. (In the absence of

the enzyme or sulfur, the cyanide may form cyano-hemoglobin.)

 

In cancer patients some thiocyanate finds its way to the site of the

cancer lesion.

 

The benzaldehyde formed in the intestine probably has no important

function, but in the circulation forms benzoic acid and is excreted

as benzaldehyde hippurate.

 

Prunasin (the mono-glucoside of Mandelonitrile) can circulate in the

body and reach the malignant lesion, and as such hydrolyse to

liberate hydrocyanic acid, benzaldehyde, and one glucose molecule.

 

Prunasin may also be changed in the liver to Mandelonitrile

glucuronoside. This conversion to the glucuoronoside may take place

in two different ways: 1) by combining with glucuronic acid, which

would remove one sugar molecule; 2) by oxidation of the terminal

alcohol group of the prunasin glucose molecule.

 

The mandelonitrile is absorbed from the intestine, going directly to

the liver where it is converted by the detoxification mechanism of

joining it to glucuronic acid. It may then be excreted as the

glucuronide or find its way to the site of a malignant lesion.

 

Glucosidic enzymes at the lesion may hydrolyse prunasin into its

components cyanide, benzaldehyde, and a glucose molecule, to

interfere with tissue respiration. In the process of enzyme

hydrolysis pure mandelonitrile, as an intermediate step, may be

released.

 

Mandelonitrile of itself may undergo spontaneous hydrolysis to HCN

and benzaldehyde or enzymatic decomposition by benzocyanase present

in the emulsin complex.

 

Mandelonitrile glucuronide may be hydrolysed at the tumor site by

Beta-glucuronidase to yield HCN, benzaldehyde and glucuronic acid.

 

Benzaldehyde released through these processes at the site of the

malignant lesion may be reduced to benzyl alcohol, and combine with

the thiocyanate to form benzo thiocyanate. This compound is further

reduced to a thio-alcohol, benzo mercaptain, and hydrocyanic acid.

In this manner HCN reappears and may continue to do so in a cyclic

manner until the intracellular conditions that permit the reaction

involved in the cycle are no longer operative.

 

These phenomena would explain the synergistic effect of benzaldehyde

and cyanide in depressing the metabolism of mouse tumor slices in

the Warburg apparatus (Dean Burk3).

 

In the absense of rhodanese the cyanide probably exerts its lethal

effects on cell respiration, which is relatively small in cancer

cells, by interferance with the cytochrome oxidase enzymes.

 

Cyanide, either as such, or as mandelonitrile, may combine with

glucose to form cyanoglucose, which, on hydrolysis, forms a

glucuronide heptose analogous to gluconic acid, which would be

excreted, or dehydrogenated to heptose, which also would be

excreted. The conditions for this transformation exist in cancer

tissue and would constitute anti-gluconeogenesis.

 

[From Physicians Handbook of Vitamin B-17 Therapy, McNaughton

Foundation, Published by: Science Press International, 1973]

 

 

http://www.navi.net/~rsc/gurchot.htm

 

References:

 

Sorbo, Acta Chem.Scand. 5,1951,(724-34);1953 (1129-1136);1953 (1137-

1145).

Clemedson et al, Acta Physiol.Scand. 32, 1954, 245.

Burk, McNaughton, Von Ardenne, PanMinerva Med.13,#12,Dec.1971.

 

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