171
Views
38
CrossRef citations to date
0
Altmetric
Original Article

Oxidative stress in myotonic dystrophy type 1

, , , , , , , , & show all
Pages 771-776 | Received 12 Feb 2005, Published online: 07 Jul 2009

References

  • Mankodi A, Thornton CA. Myotonic syndromes. Curr Opin Neurol 2002;15:545–552.
  • Ranum LPW, Day JW. Dominantly inherited, non-coding micro-satellite expansion disorders. Curr Opin Genet Dev 2002; 12:266–271.
  • Ranum LPW, Day JW. Myotonic dystrophy: RNA pathogene-sis comes into focus. Am J Hum Genet 2004;74:793–804.
  • Day JW, Ranum LPW. RNA pathogenesis of the myotonic dystrophies. Neuromuscul Disord 2005;15:5–16.
  • Philips AV, Timchenko LT, Cooper TA. Disruption of slicing regulated by a CUG-binding protein in myotonic dystrophy. Science 1998;280:737–741.
  • Groenen P, Wieringa B. Expanding complexity in myotonic dystrophy. Bioessays 1998;20:901 —912.
  • Goldstein S. Human genetic disorders that feature premature onset and accelerated progression of biological aging. In: Schneider EL, editor. The genetics of aging. New York: Plenum Press; 1978.
  • Ihara Y, Mori A, Hayabara T, et al. Free radicals, lipid peroxides and antioxidants in blood of patients with myotonic dystrophy. J Neurol 1995;242:119–122.
  • Usuki F, Ishiura S. Expanded CTG repeats in myotonin protein kinase increase the susceptibility to oxidative stress. Neuroreport 1998;9:2291–2296.
  • Usuki F, Takahashi N, Sasagawa N, Ishiura S. Differential signaling pathways following oxidative stress in mutant myotonin protein kinase cDNA-transfected C2C12 cell lines. Biochem Byophys Res Commun 2000;267:739–743.
  • Griggs, R.C., Wood, D.S. and the Working Group on the Molecular Defect in Myotonic Dystrophy Criteria for establishing the validity of genetic recombination in myotonic dystrophy. Neurology 1992;42:2030–2082.
  • Mahadevan M, Tsilfidis C, Sabourin L, et al. Myotonic dystrophy mutation: An unstable CTG repeat in the 31 untranslated region of the gene. Science 1992;255:1253–1255.
  • Nieremberg DW, Lester DC. Determination of vitamins E and A in serum and plasma using a simplified clarification method and high-performance liquid chromatography. J Chromatogr 1985;345:275–284.
  • Floyd RA, Watson JJ, Wong PK. Sensitive assay of hydroxyl free radical formation utilizing high pressure liquid chromatography with electrochemical detection of phenol and salicylate products. J Biochem Biophys Methods 1984;10:221–235.
  • Takemura G, Onodera T, Ashraf M. Quantification of hydroxyl radical and its lack of relevance to myocardial injury during early reperfusion after graded ischemia in rat heart. Circ Res 1992;71:96–105.
  • Onodera T, Asharaf M. Detection of hydroxyl radicals in the post-ischemic reperfused heart using salicylate as a trapping agent. J Mol Cell Cardiol 1991;23:365–370.
  • Moosmann B, Behl C. Antioxidants as treatment for neurodegenerative disorders. Expert Opin Investig Drugs 2002;11:1407–1435.
  • Guentchev M, Siedlak SL, Janus C, Tagliavini F, Castellani RJ, Perry G, Smith MA, Budka G. Oxidative damage to nucleic acids in human prion disease. Neurobiol Dis 2002;9:275–281.
  • Pattee GL, Post GR, Gerber RE, Bennett JP. Reduction of oxidative stress in amyotrophic lateral sclerosis following pramipexole treatment. Amyotroph Lateral Sc 2003;4:90.
  • Pitkanen S, Robinson BH. Mitochondrial complex I deficiency leads to increased production of superoxide radicals and induction of superoxide dismutase. J Clin Invest 1996;15: 345–351.
  • Rodriguez MC, Tarnopolsky MA. Patients with dystrophino-pathy show evidence of increased oxidative stress. Free Radic Biol Med 2003;34:1217–1220.
  • Mankodi A, Logigian E, Callahan L, McClain C, White R, Henderson D, Krym M, Thorton CA. Myotonic dystrophy in trangenic mice expressing an expanded CUG repeat. Science 2000;289:1769–1773.
  • Seznec H, Agbulut 0, Sergeant N, Savouret C, Ghestem A, Tabti N, et al. Mice transgenic for the human myotonic dystrophy region with expanded CTG repeats display muscular and brain abnormalities. Hum Mol Genet 2001;10:2717–2726.
  • Hsiao KK, Borchelt DR, Olson K, Johannsdottir R, Kitt C, Yunis W, Xu S, Eckman C, Younkin S, Price D, Iadecola C, Clark HB, Carlson G, et al. Age-related CNS disorder and early death in transgenic FVB/N mice overexpressing Alzheimer amyloid precursor proteins. Neuron 1995;15:1203–1218.
  • Klement IA, Skinner PJ, Kaytor MD, Yi H, Hersch SM, Clark HB, Zoghbi HY, Orr HT. Ataxin-1 nuclear localization and aggregation: Role in polyglutamine-induced disease in SCA1 trangenic mice. Cell 1998;95:41–53.
  • Graf M, Ecker D, Horowski R, Kramer B, Riederer P, Gerlach M, et al. High dose vitamin E theraphy in amyotrophic lateral sclerosis as add-on theraphy to riluzole: Results of a placebo-controlled double-blind study. J Neural Transm 2004; Oct 27.
  • Maiese K, Chong ZZ. Insights into oxidative stress and potential novel therapeutic targets for Alzheimer disease. Neurol Neumsci 2004;22:87–104.
  • Gille G, Hung ST, Reichmann H, Rausch WD. Oxidative stress to dopaminergic neurons as models of Parkinson's disease. NY Acad Sci 2004;1018:533–540.
  • Furling D, Doucet G, Langlois MA, Timchenko L, Belanger E, Cossette L, Puymirat J. Viral vector producing antisense RNA restores myotonic dystrophy myoblast functions. Gene Ther 2003;10:795–802.
  • Langlois MA, Lee NS, Rossi JJ, Puymirat J. Hammerhead ribozyme-mediated destruction of nuclear foci in myotonic dystrophy myoblasts. Mol Ther 2003;7:670–680.

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.