Incredible edible egg!!
http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0042017 Taurine Provides Neuroprotection against Retinal Ganglion Cell Degeneration Abstract <http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0042017#top> Retinal ganglion cell (RGC) degeneration occurs in numerous retinal diseases leading to blindness, either as a primary process like in glaucoma, or secondary to photoreceptor loss. However, no commercial drug is yet directly targeting RGCs for their neuroprotection. In the 70s, taurine, a small sulfonic acid provided by nutrition, was found to be essential for the survival of photoreceptors, but this dependence was not related to any retinal disease. More recently, taurine deprivation was incriminated in the retinal toxicity of an antiepileptic drug. We demonstrate here that taurine can improve RGC survival in culture or in different animal models of RGC degeneration. Taurine effect on RGC survival was assessed *in vitro* on primary pure RCG cultures under serum-deprivation conditions, and on NMDA-treated retinal explants from adult rats. *In vivo*, taurine was administered through the drinking water in two glaucomatous animal models (DBA/2J mice and rats with vein occlusion) and in a model of *Retinitis pigmentosa* with secondary RGC degeneration (P23H rats). After a 6-day incubation, 1 mM taurine significantly enhanced RGCs survival (+68%), whereas control RGCs were cultured in a taurine-free medium, containing all natural amino-acids. This effect was found to rely on taurine-uptake by RGCs. Furthermore taurine (1 mM) partly prevented NMDA-induced RGC excitotoxicity. Finally, taurine supplementation increased RGC densities both in DBA/2J mice, in rats with vein occlusion and in P23H rats by contrast to controls drinking taurine-free water. This study indicates that enriched taurine nutrition can directly promote RGC survival through RGC intracellular pathways. It provides evidence that taurine can positively interfere with retinal degenerative diseases. *Citation: *Froger N, Cadetti L, Lorach H, Martins J, Bemelmans A-P, et al. (2012) Taurine Provides *Figure 5. <http://www.plosone.org/article/info:doi/10.1371/journal.pone.0042017?imageURI=info:doi/10.1371/journal.pone.0042017.g005> Taurine supplementation prevents RGC degeneration in glaucomatous Long-Evans rats following episcleral vein occlusion.* ** Taurine Reduces the Secondary RGC Degeneration Following Photoreceptor Loss in P23H Rats *Taurine was previously reported to prevent glutamate excitotoxicity in embryonic cultured cerebellar neurons [11]<http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0042017#pone.0042017-ElIdrissi1>or mixed brain neurons [10]<http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0042017#pone.0042017-Wu1>. Our present study extends this conclusion to adult RGCs in NMDA-treated retinal explants. *The intracellular effects of taurine discussed above could explain this prevention of RGC glutamate excitotoxicity in NMDA-treated retinal explants. Especially, the taurine-induced reduction of intracellular Ca2+ levels, as described in brain neurons [10]<http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0042017#pone.0042017-Wu1>, [11]<http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0042017#pone.0042017-ElIdrissi1>and in immortalized RGCs under hypoxia [20]<http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0042017#pone.0042017-Chen1>, could limit the toxic Ca2+ overload resulting from the prolonged activation of the Ca2+-permeable NMDA receptors. The taurine-mediated reduction in glutamate excitotoxicity could also be attributed to the taurine effect on glutamate uptake [31]<http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0042017#pone.0042017-Chen2>. Despite the negative conclusion of the clinical trial with memantine, a blocker of NMDA receptors [32]<http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0042017#pone.0042017-DaneshMeyer1>, glutamate excitotoxicity is considered as an important molecular mechanism in RGC degeneration during glaucoma and other retinal diseases with an ischemic contribution [21]<http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0042017#pone.0042017-Seki1>. Therefore, the protective effect of taurine on pure RGC cultures and on RGC glutamate excitotoxicity could explain the *in vivo* RGC rescue in glaucoma animal models. [Non-text portions of this message have been removed] |
well its an extra can of red bull for me today then !
puk In a message dated 19/11/2012 04:39:45 GMT Standard Time, [hidden email] writes: Incredible edible egg!! _http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0042017_ (http://www.plosone.org/article/info:doi/10.1371/journal.pone.0042017) Taurine Provides Neuroprotection against Retinal Ganglion Cell Degeneration Abstract <_http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0042017#top_ (http://www.plosone.org/article/info:doi/10.1371/journal.pone.0042017#top) > Retinal ganglion cell (RGC) degeneration occurs in numerous retinal diseases leading to blindness, either as a primary process like in glaucoma, or secondary to photoreceptor loss. However, no commercial drug is yet directly targeting RGCs for their neuroprotection. In the 70s, taurine, a small sulfonic acid provided by nutrition, was found to be essential for the survival of photoreceptors, but this dependence was not related to any retinal disease. More recently, taurine deprivation was incriminated in the retinal toxicity of an antiepileptic drug. We demonstrate here that taurine can improve RGC survival in culture or in different animal models of RGC degeneration. Taurine effect on RGC survival was assessed *in vitro* on primary pure RCG cultures under serum-deprivation conditions, and on NMDA-treated retinal explants from adult rats. *In vivo*, taurine was administered through the drinking water in two glaucomatous animal models (DBA/2J mice and rats with vein occlusion) and in a model of *Retinitis pigmentosa* with secondary RGC degeneration (P23H rats). After a 6-day incubation, 1 mM taurine significantly enhanced RGCs survival (+68%), whereas control RGCs were cultured in a taurine-free medium, containing all natural amino-acids. This effect was found to rely on taurine-uptake by RGCs. Furthermore taurine (1 mM) partly prevented NMDA-induced RGC excitotoxicity. Finally, taurine supplementation increased RGC densities both in DBA/2J mice, in rats with vein occlusion and in P23H rats by contrast to controls drinking taurine-free water. This study indicates that enriched taurine nutrition can directly promote RGC survival through RGC intracellular pathways. It provides evidence that taurine can positively interfere with retinal degenerative diseases. *Citation: *Froger N, Cadetti L, Lorach H, Martins J, Bemelmans A-P, et al. (2012) Taurine Provides *Figure 5. <_http://www.plosone.org/article/info:doi/10.1371/journal.pone.0042017?image URI=info:doi/10.1371/journal.pone.0042017.g005_ (http://www.plosone.org/article/info:doi/10.1371/journal.pone.0042017?imageURI=info:doi/10.1371/journal. pone.0042017.g005) > Taurine supplementation prevents RGC degeneration in glaucomatous Long-Evans rats following episcleral vein occlusion.* ** Taurine Reduces the Secondary RGC Degeneration Following Photoreceptor Loss in P23H Rats *Taurine was previously reported to prevent glutamate excitotoxicity in embryonic cultured cerebellar neurons [11]<_http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.004 2017#pone.0042017-ElIdrissi1_ (http://www.plosone.org/article/info:doi/10.1371/journal.pone.0042017#pone.0042017-ElIdrissi1) >or mixed brain neurons [10]<_http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.004 2017#pone.0042017-Wu1_ (http://www.plosone.org/article/info:doi/10.1371/journal.pone.0042017#pone.0042017-Wu1) >. Our present study extends this conclusion to adult RGCs in NMDA-treated retinal explants. *The intracellular effects of taurine discussed above could explain this prevention of RGC glutamate excitotoxicity in NMDA-treated retinal explants. Especially, the taurine-induced reduction of intracellular Ca2+ levels, as described in brain neurons [10]<_http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.004 2017#pone.0042017-Wu1_ (http://www.plosone.org/article/info:doi/10.1371/journal.pone.0042017#pone.0042017-Wu1) >, [11]<_http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.004 2017#pone.0042017-ElIdrissi1_ (http://www.plosone.org/article/info:doi/10.1371/journal.pone.0042017#pone.0042017-ElIdrissi1) >and in immortalized RGCs under hypoxia [20]<_http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.004 2017#pone.0042017-Chen1_ (http://www.plosone.org/article/info:doi/10.1371/journal.pone.0042017#pone.0042017-Chen1) >, could limit the toxic Ca2+ overload resulting from the prolonged activation of the Ca2+-permeable NMDA receptors. The taurine-mediated reduction in glutamate excitotoxicity could also be attributed to the taurine effect on glutamate uptake [31]<_http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.004 2017#pone.0042017-Chen2_ (http://www.plosone.org/article/info:doi/10.1371/journal.pone.0042017#pone.0042017-Chen2) >. Despite the negative conclusion of the clinical trial with memantine, a blocker of NMDA receptors [32]<_http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.004 2017#pone.0042017-DaneshMeyer1_ (http://www.plosone.org/article/info:doi/10.1371/journal.pone.0042017#pone.0042017-DaneshMeyer1) >, glutamate excitotoxicity is considered as an important molecular mechanism in RGC degeneration during glaucoma and other retinal diseases with an ischemic contribution [21]<_http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.004 2017#pone.0042017-Seki1_ (http://www.plosone.org/article/info:doi/10.1371/journal.pone.0042017#pone.0042017-Seki1) >. Therefore, the protective effect of taurine on pure RGC cultures and on RGC glutamate excitotoxicity could explain the *in vivo* RGC rescue in glaucoma animal models. [Non-text portions of this message have been removed] [Non-text portions of this message have been removed] |
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