Biosynthesis Lab Report

B) Site of synthesis:
1- In pancreas: Synthesis of taurine in the mammalian pancreas occurs through the cysteine sulfinic acid pathway. First, in this pathway is oxidation of cysteine sulfahydryl group to sulfonic acid, this oxidation is catalyzed by the enzyme cysteine dioxygenase. In turn, cysteine sulfonic acid is decarboxylated to hypotaurine by sulfonoalanine decarboxylase. It is not well known whether hypotaurine is then enzymatically or spontaneously oxidized to taurine.
2- in CNS:
Biosynthesis of taurine in CNS occurs via four routes.
1- Cysteine sulfonic acid (CSA) Decarboxylase route:
It is the most accepted route in the CNS. It includes cysteine, CSA, hypotaurine and taurine as a metabolic sequence.
2- Cystine dioxygenase route:
Cellular transport of taurine is sodium dependant. The ratio of sodium molecules to taurine molecule transported varies in different tissues ranging from 3:1 to 1:1.Transport of taurine in brain require at least 3 Na+ molecules, transport of hypotaurine require 2 Na+ molecules. Transport of taurine takes place in both neurons and glial cells. The transport in glial cells is greater than neurons and astrocytes. Deficiency of taurine stimulates retinal transport of taurine. The sites in mammalian retina where taurine transport is concentrated are, pigment epithelium, photoreceptors and neuronal amoxine cells. o In mammalian retina taurine transport is concentrated in neuronal amoxine cell and photoreceptor and pigment epithelium. It was found that taurine transport fall by 72% if the pigment epithelium was removed from choroid. In human transport of taurine across the pigment epithelia is required for maintaining electrophysiological function of retina.
Taurine release
There are three ways for cellular release of taurine:
The first way is the basal release by leakage of taurine through the cell membrane. The second way is taurine release by reversal of active transport
Production of proinflammatory cytokines such as: tumor necrosing factor alpha, interleukin 1 and unterleukin 6) is inhibited by taurine. Also taurine chloramine decreases the production of nitric oxide(NO) and prostaglandind E2(PGE2). These effects in addition to the ability of TauCl to induce leukocytes apoptosis, demonstrate the ability of TauCl cto terminate acute inflammatory condition. Also TauCl and TauBr depress the phagocytic cell activity and decrease phagocytic cell oxygen consumption and production of respiratory burst. TauCl also, increases the expression of peroxyredoxin-1 and thioredoxin-1, which in turn cause decrease in ROS production. TauCl and TauBr significantly increase the expression of heme oxygenase-1 (HO-1) in dose dependent manner. HO-1 has special role in homeostasis as HO-1 decrases the synthesis of priinflammatory heme portion as: cyclocoxygenase (COX-2) and inducible nitric oxide synthase (iNOS). Therefore, TauCl and TauBr induce HO-1 in nearby non activated cells and protect these cells against hazards of oxidative