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Functional Assessment of Urinary Neuro-biogenic Amines—A COMPREHENSIVE GUIDE 

49

Detoxification

One of the liver’s primary functions

is the detoxification of xenobiotics (for-

eign compounds) so they may be excret-

ed in urine or bile. Three phases of de-

toxification occur:

Phase I detoxification occurs as

cytochrome P450, oxidase, reductase

and dehydrogenase enzymes add a

hydroxyl group (-OH) onto organic

compounds. This step converts

fat-soluble compounds into water-

soluble compounds.

Toxic metals such as arsenic,

cadmium, mercury and lead

may inhibit cytochrome P450

enzymes

Urine Toxic Metals Whole Blood Elements

– Heme is incorporated into all

cytochrome P450 enzymes

– Heme is synthesized by the

porphyrin pathway. The

porphyrin pathway may be

evaluated in the laboratory:

Urine Porphyrins

Xenobiotics activated by phase

I may generate reactive oxygen

species and increase oxidative

stress

Lipopolysaccharides and

peptidoglycans from

gastrointestinal bacteria, if

released into the circulation

may contribute to neural

inflammation in the central

nervous system and may

downregulate liver phase I

detoxification. (See

Digestion

and Absorption

section.)

Digestion and absorption may be

evaluated in the laboratory:

Comprehensive Stool Analysis Intestinal Permeability

Nutrients that may support

phase I include selenium,

zinc and vitamins A, D, E,

K, and C. Plant compounds,

such as sulforaphanes found

in broccoli and other Brassica

family vegetables also support

detoxification.

Red Blood Cell (RBC) Elements

Phase II detoxification occurs

through a variety of different

reactions including glucuronidation,

sulfation, methylation,

N-acetylation, and conjugation with

amino acids or the attachment of

glutathione.

Phase II conjugation may be

inhibited by arsenic, cadmium,

lead, mercury and hexavalant

chromium which inhibit the

enzyme glutathione S-transferase

(GST).

– An isoform of GST found

in neurons prevents

neurodegeneration.

Glutathione (GSH) needs to be

available for the GST enzyme

to function; low levels of

GSH may occur if synthesis is

compromised by enzyme defects

or if there are enzyme defects in

the methylation pathway. (See

Methylation

section.)

– GSH is the primary

antioxidant in the body. Low

levels predispose cells towards

oxidative stress. Oxidative

stress is a contributing factor

to neurodegeneration.

Nutrients that may support phase

II include reduced glutathione,

N-acetyl cysteine (glutathione