Neuroprotective effect of taurine in 3-nitropropionic acid-induced experimental animal model of Huntington's disease phenotype

Tadros, Mariane G.; Khalifa, Amani E.; Abdel-Naim, Ashraf B.; Arafa, Hossam M.M.

doi:10.1016/j.pbb.2005.10.018

Cited by 71 publications

(38 citation statements)

References 40 publications

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“…This suggests that the administration of antioxidants should be considered as an adjuvant therapy for patients. Along these lines, taurine was shown to be beneficial in prolonging lifespan in the SSADH-deficient mouse model , and taurine has antioxidant properties (Kaplan et al 2004;Tadros et al 2005). Taken together, evaluation of antioxidant intervention would now seem warranted in both human and murine SSADH deficiency.…”

Section: Discussionmentioning

confidence: 99%

Evidence for oxidative stress in tissues derived from succinate semialdehyde dehydrogenase‐deficient mice

Latini

Scussiato

Leipnitz

et al. 2007

J of Inher Metab Disea

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Animal models of inborn errors of metabolism are useful for investigating the pathogenesis associated with the corresponding human disease. Since the mechanisms involved in the pathophysiology of succinate semialdehyde dehydrogenase (SSADH) deficiency (Aldh5a1; OMIM 271980) are still not established, in the present study we evaluated the tissue antioxidant defences and lipid peroxidation in various cerebral structures (cortex, cerebellum, thalamus and hippocampus) and in the liver of SSADH-deficient mice. The parameters analysed were total radical-trapping antioxidant potential (TRAP) and glutathione (GSH) levels, the activities of the antioxidant enzymes superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx), as well as thiobarbituric acid-reactive substances (TBARS). We first observed that the tissue nonenzymatic antioxidant defences were significantly reduced in the SSADH-deficient animals, particularly in the liver (decreased TRAP and GSH) and in the cerebral cortex (decreased GSH), as compared to the wild-type mice. Furthermore, SOD activity was significantly increased in the liver and cerebellum, whereas the activity of CAT was significantly higher in the thalamus. In contrast, GPx activity was significantly diminished in the hippocampus. Finally, we observed that lipid peroxidation (TBARS levels) was markedly increased in the liver and cerebral cortex, reflecting a high lipid oxidative damage in these tissues. Our data showing an imbalance between tissue antioxidant defences and oxidative attack strongly indicate that oxidative stress is involved in the pathophysiology of SSADH deficiency in mice, and likely the corresponding human disorder.

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Section: Discussionmentioning

confidence: 99%

Evidence for oxidative stress in tissues derived from succinate semialdehyde dehydrogenase‐deficient mice

Latini

Scussiato

Leipnitz

et al. 2007

J of Inher Metab Disea

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show abstract

“…Taurine was first shown to be capable of improving osmotic status and calcium homeostasis in cell damage caused by hypoxia or glutamate excitotoxicity (Chang et al 2004;Idrissi and Trenkner 1999;Michalk et al 1997).As an antioxidant, taurine protects tissues against reactive oxygen species generation from hypoxia or from Mn-superoxide dismutase inhibition in the myocardial mitochondria (Chen et al 2009). In addition, taurine is also a GABA agonist and may increase GABA levels by increasing GABA synthesis and by GABAA receptor activation (Paula-Lima et al 2005;Tadros et al 2005). Several papers provided the evidence that taurine exerts protective effects through prevention of mitochondrial dysfunction (Chang et al 2004;Chen et al 2009;Hansen et al 2010).…”

Section: Discussionmentioning

confidence: 99%

“…Taurine has been applied to treat multiple neurological diseases including Alzheimer's disease, Huntington's disease, brain ischemia and heart ischemia (Paula-Lima et al 2005;Tadros et al 2005;Takahashi et al 2003;Takatani et al 2004b). However, the mechanisms underlying the functions of taurine are still not fully understood.…”

Section: Introductionmentioning

confidence: 99%

Beneficial effect of taurine on hypoxia- and glutamate-induced endoplasmic reticulum stress pathways in primary neuronal culture

et al. 2011

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Stroke (hypoxia) is one of the leading causes of mortality in the developed countries, and it can induce excessive glutamate release and endoplasmic reticulum (ER) stress. Taurine, as a free amino acid, present in high concentrations in a range of organs in mammals, can provide protection against multiple neurological diseases. Here, we present a study to investigate the potential protective benefits of taurine against ER stress induced by glutamate and hypoxia/reoxygenation in primary cortical neuronal cultures. We found that taurine suppresses the up-regulation of caspase-12 and GADD153/CHOP induced by hypoxia/reoxygenation, suggesting that taurine may exert a protective function against hypoxia/reoxygenation by reducing the ER stress. Moreover, taurine can down-regulate the ratio of cleaved ATF6 and full length ATF6, and p-IRE1 expression, indicating that taurine inhibits the ER stress induced by hypoxia/reoxygenation and glutamate through suppressing ATF6 and IRE1 pathways.

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“…Recently, for example, protection was seen in 3-NP models of HD using the β-amino acid taurine, which has antioxidant and γ-aminobutyric acid (GABA)-ergic properties, and celastrol, which has antioxidant, anti-inflammatory, and antiaggregation properties and is extracted from a Chinese vine used in traditional medicine [34,35]. It remains to be seen, however, whether these will continue to show promise in clinical studies.…”

Section: Therapies Targeting Mitochondrial Dysfunction Excitotoxicitmentioning

confidence: 99%

Update on huntington’s disease

Berman¹,

Greenamyre

2006

Curr Neurol Neurosci Rep

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Huntington's disease (HD) is a devastating neurodegenerative disease causing progressive movement disorders, cognitive dysfunction, and behavioral changes. Since the causative mutation of an expanded polyglutamine repeat in the huntingtin gene was identified, significant progress has been achieved in elucidating pathogenic mechanisms. This review summarizes recent developments in evaluating the role of abnormal protein aggregation, transcriptional dysregulation, mitochondrial and bioenergetic dysfunction, excitotoxicity, and abnormal cellular trafficking in the pathogenesis of HD. In addition, although therapeutic options in HD have been limited, progress in developing targeted therapies continues, and these advancements and future directions are reviewed.

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Neuroprotective effect of taurine in 3-nitropropionic acid-induced experimental animal model of Huntington's disease phenotype

Cited by 71 publications

References 40 publications

Evidence for oxidative stress in tissues derived from succinate semialdehyde dehydrogenase‐deficient mice

Evidence for oxidative stress in tissues derived from succinate semialdehyde dehydrogenase‐deficient mice

Beneficial effect of taurine on hypoxia- and glutamate-induced endoplasmic reticulum stress pathways in primary neuronal culture

Update on huntington’s disease

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