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

Taurine: a conditionally essential amino acid

in humans? An overview in health and


Nutr. Hosp. (2002) XVII (6) 262-270


S.V.R. 318

Lu, Cai-Ling; Tang, Shen; Meng, Zhi-Juan;

He, Yi-Yuan; Song, Ling-Yong et al.


Taurine improves the spatial learning and

memory ability impaired by sub-chronic

manganese exposure.

Journal of biomedical science

vol. 21 p. 51

Menzie, Janet; Pan, Chunliu; Prentice,

Howard; Wu, Jang-Yen (2014)

Taurine and central nervous system


Amino acids

vol. 46 (1) p. 31-46

Ripps, Harris; Shen, Wen (2012)

Review: taurine: a “very essential” amino


Molecular vision

vol. 18 p. 2673-86

Stipanuk, M H; Ueki, I; Dominy, J E;

Simmons, C R; Hirschberger, L L (2009)

Cysteine dioxygenase: a robust system for

regulation of cellular cysteine levels.

Amino acids

vol. 37 (1) p. 55-63

Ueki, Iori; Stipanuk, Martha H. (2007)

Enzymes of the Taurine Biosynthetic

Pathway Are Expressed in Rat Mammary


J. Nutr.

vol. 137 (8) p. 1887-1894

Taurine biosynthesis by neurons and


Vitvitsky, Victor; Garg, Sanjay K; Banerjee,

Ruma (2011)

The Journal of biological chemistry

vol. 286

(37) p. 32002-10


Glycine is a non-essential dietary

amino acid. Glycine signaling contrib-

utes to a variety of motor and sensory

functions, primarily pain perception.

Glycine has an inhibitory effect when

binding to glycine receptors in the spi-

nal cord, brainstem or retina, and is con-

sidered inhibitory in the CNS, though

glycine synapses may be excitatory in

the immature brain (animal studies).

In the brain, glycine is an essential co-

factor with glutamate for N-methyl-D-

aspartate (NDMA) receptor excitatory

signaling. The release of glycine by glial

cells and the presence of glycine trans-

porters on those cells suggest that gly-

cine may also act as a neuromodulator.


Decreased urinary glycine may occur

due to impaired renal clearance or tox-

icant exposure. Glycine is required for

glutathione synthesis and purine syn-

thesis for DNA or RNA. Glycine does

not cross the blood brain barrier easily.

Endogenous and xenobiotic organic ac-

ids and aromatic acids are conjugated to

glycine for excretion in the urine. In the

CNS, glycine conjugation occurs in the

mitochondria and provides a mechanism

to remove aromatic acid toxicants such

as benzoic acid. Glycine supplements

have been used to improve sleep quality

and used in conjunction with pharma-

ceutical supports for schizophrenia.

Excess glycine is metabolized by the

mitochondria using the enzyme glycine

decarboxylase into 5,10,-methylene

tetrahydrofolate, CO-2 and ammonia.

Glycine decarbooxylase is common-

ly called the glycine cleavage complex

(GCC); it is comprised of four different

proteins and requires pyridoxal phos-

phate (B-6) and tetrahydrofolate cofac-

tors. Genetic defects in the GCC may

result in glycine encephalopathy. This

condition is characterized by nonketot-

ic hyperglycinemia (NKH) and elevated

urinary glycine. Animal studies indicate

that elevated glycine levels may severely