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cysteic acid

Figure 14.7. Pathways for the synthesis of taurine from cysteine. Cysteine sulfinate decarboxylase, EC 4.1.1.29; cysteic acid decarboxylase, EC 4.1.1.29 (glutamate decarboxylase, EC 4.1.1.15); cysteine oxidase, EC 1.13.11.20; cysteamine oxygenase, EC 1.13.11.19 and hypotaurine oxidase, EC 1.8.1.3. Relative molecular masses (Mr): cysteine, 121.2 cysteamine, 77.2; cysteine sulfinic acid, 153.2; cysteic acid, 169.2; hypotaurine, 109.1 and taurine, 125.1.

of cysteine sulfinic acid that is rate-limiting for taurine synthesis, not the oxidation of cysteine.

2. Oxidation to cysteic acid, followed by decarboxylation to taurine. Cysteic acid and cysteine sulfinic acid decarboxylase activities occur in constant ratio in various tissues, and it is likely that both substrates are decarboxy-lated by the same enzyme. In general, cysteine sulfinic acid is the preferred substrate, and there is little formation of taurine by way of cysteic acid.

3. S-Oxidation of cysteamine released by the catabolism of pantothenic acid (Section 12.2.2) or formed by the decarboxylation of cysteine.

In the liver and brain, the main pathway is by way of cysteine sulfinic acid, whereas in tissues with low cysteine sulfinic acid decarboxylase activity the main precursor of taurine is cysteamine.

The central nervous system has at least three enzymes capable of decar-boxylating cysteine sulfonic acid, one of which is glutamate decarboxylase. Glutamate and cysteine sulfinic acid are mutually competitive. In some brain regions, more than half the total cysteine sulfinic acid decarboxylase activity may be from glutamate decarboxylase.

In addition to taurocholic acid in the bile, free taurine is excreted in the urine. At times of low intake or when synthesis is impaired, for example by vitamin B6 deficiency, the renal tubular resorption of taurine is increased, thus reducing urinary losses.

Feeding experimental animals on high taurine diets results in increased urinary excretion, but has little or no effect on endogenous synthesis.

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