Most-abundant free amino acid in mammals; not protein-bound. Synthesized from cysteine: cysteine → cysteine sulfinic acid (via cysteine dioxygenase, CDO1) → hypotaurine (via cysteine sulfinic acid decarboxylase, CSAD, the rate-limiting step) → taurine (via hypotaurine dehydrogenase). Major uses: (1) bile-acid conjugation (cholic + chenodeoxycholic acid + taurine → taurocholate / taurochenodeoxycholate, ratio 1:3 with glycine conjugates in humans); (2) osmolyte in retinal photoreceptors + cardiomyocytes; (3) GABA-A receptor agonist (CNS inhibition); (4) cardioprotection (taurine deficiency in cats → dilated cardiomyopathy, a classic veterinary observation that drove discovery of taurine essentiality in cats). Humans can synthesize but at low rates — supplemental taurine is investigated for CHF, post-MI cardioprotection, and as a popular component of energy drinks (proposed efferent + glycemic effects).
Organ Systems
digestive
nervous
Pathway Steps
cysteine → cysteine-sulfinic-acid — via cysteine dioxygenase (CDO1). Cysteine dioxygenase commits cysteine toward taurine (vs glutathione or H2S) and is strongly regulated by cysteine availability, protecting against cysteine toxicity — the gateway to the taurine branch of sulfur-amino-acid metabolism.
cysteine-sulfinic-acid → hypotaurine — via cysteine sulfinic acid decarboxylase (CSAD) — RATE-LIMITING. CSAD (PLP/B6-dependent) is the rate-limiting taurine-synthesis enzyme; humans synthesize taurine slowly (and cats lack CSAD entirely), making it conditionally essential — hence taurine in infant formula and its abundance in animal foods.
hypotaurine → taurine — via hypotaurine dehydrogenase. Hypotaurine is oxidized to taurine, among the most abundant free amino acids — used in bile-salt (taurocholate) conjugation, osmoregulation, membrane/Ca²⁺ stabilization, and antioxidant defense in heart and retina.