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.