Weekly Wellness Spotlight

Dear Julie,


Taurine is synthesized by humans from cysteine in a process that requires vitamin B6. It exists in the body as a free amino acid, and it is not used for protein synthesis. Taurine stabilizes cell membranes, functions as a neurotransmitter and osmoregulator, is involved in conjugation of bile acids, and plays a role in retinal function. Retinal taurine is crucial in preventing RGC damage in major retinal diseases. Orally administered taurine is well-absorbed. Taurine is present exclusively in animal foods. Cats, which (unlike humans) have little capacity to synthesize taurine, develop retinal degeneration when fed a taurine-deficient diet.
Taurine-deficient monkeys have morphological changes in photoreceptors and impaired visual acuity. Other potential consequences of suboptimal taurine status include decreased cardiac contractility, increased susceptibility to cardiac arrhythmias, platelet hyperaggregability, and inefficient fat digestion. See the articles below on taurine and consider the implications of its addition to neutraceuticals.


Taurine: The comeback of a neutraceutical in the prevention of retinal degenerations

Taurine is the most abundant amino acid in the retina. In the 1970s, it was thought to be involved in retinal diseases with photoreceptor degeneration, because cats on a taurine-free diet presented photoreceptor loss. However, with the exception of its introduction into baby milk and parenteral nutrition, taurine has not yet been incorporated into any commercial treatment with the aim of slowing photoreceptor degeneration. Our recent discovery that taurine depletion is involved in the retinal toxicity of the antiepileptic drug vigabatrin has returned taurine to the limelight in the field of neuroprotection. However, although the retinal toxicity of vigabatrin principally involves a deleterious effect on photoreceptors, retinal ganglion cells (RGCs) are also affected. These findings led us to investigate the possible role of taurine depletion in retinal diseases with RGC degeneration, such as glaucoma and diabetic retinopathy. The major antioxidant properties of taurine may influence disease processes. In addition, the efficacy of taurine is dependent on its uptake into retinal cells, microvascular endothelial cells and the retinal pigment epithelium. Disturbances of retinal vascular perfusion in these retinal diseases may therefore affect the retinal uptake of taurine, resulting in local depletion. The low plasma taurine concentrations observed in diabetic patients may further enhance such local decreases in taurine concentration. We here review the evidence for a role of taurine in retinal ganglion cell survival and studies suggesting that this compound may be involved in the pathophysiology of glaucoma or diabetic retinopathy. Along with other antioxidant molecules, taurine should therefore be seriously reconsidered as a potential treatment for such retinal diseases.  See attatched article.



Magnesium acethyltaurate as a potential agent for retinal and optic nerve protection in glaucoma

In line with the observations stated here, we have previously described the role of Mg in ophthalmic diseases (Agarwal et al., 2013, 2014). The neuroprotective effects of taurine alone are also well established. Retinal taurine level is crucial in preventing RGC damage in major retinal diseases. It was found that taurine can directly prevent RGC degeneration, occurring either in serum-deprived pure RGC cultures or in animal models representing RGC loss.
Furthermore, taurine is known to partly prevent NMDA-induced RGC excitotoxicity. Hence, MgAT, a combined salt of Mg and taurine, seems to be effective in preventing NMDA and ET-1 induced retinal and optic nerve damage by counteracting NMDA receptor activation, reducing retinal oxidative stress, increasing retinal BDNF level and reducing activation of caspase and pro-apoptotic proteins
Based on the investigations done so far, it can be concluded that MgAT has protective effects against NMDA and ET-1 induced retinal and optic nerve damage. Considering the enhanced efficacy of MgAT particularly on pre-treatment, it is likely that MgAT primarily has therapeutic potential as a protective agent in high risk individuals. Development of appropriate formulations to administer MgAT noninvasively would be the key to its clinical application. Furthermore, investigations into the mechanisms of action of MgAT will reveal its true potential as an antiglaucoma agent.