TEMPOL facilitated the development of the deep vascular layer before neural degeneration occurs in retinal degeneration (rd1) mice.
Graefes Arch Clin Exp Ophthalmol. 2014 Mar;252(3):411-6 Oxidative stress retards vascular development before neural degeneration occurs in retinal degeneration rd1 mice. Fukuda S1, Ohneda O, Oshika T. 1Department of Ophthalmology, Institute of Clinical Medicine, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki, 305-8575, Japan Abstract PURPOSE: To investigate the role of reactive oxygen species (ROS) in […]Take a Tour
Toxicol Sci. 2012 Oct;129(2):411-20. Characterization of mitophagy in the 6-hydoxydopamine Parkinson’s disease model. Solesio ME1, Saez-Atienzar S, Jordán J, Galindo MF. 1Unidad de Neuropsicofarmacología Traslacional, Complejo Hospitalario Universitario de Albacete, Albacete, Spain. Abstract In the present study, the activation of autophagy and its interaction with the mitochondrial fission machinery was investigated in an experimental model […]Take a Tour
Oxidation of the tryptophan 32 residue of human superoxide dismutase 1 caused by its bicarbonate-dependent peroxidase activity triggers the non-amyloid aggregation of the enzyme.
J Biol Chem. 2014 Oct 31;289(44):30690-701. Oxidation of the tryptophan 32 residue of human superoxide dismutase 1 caused by its bicarbonate-dependent peroxidase activity triggers the non-amyloid aggregation of the enzyme. Coelho FR1, Iqbal A1, Linares E1, Silva DF1, Lima FS1, Cuccovia IM1, Augusto O2. 1From the Departamento de Bioquímica, Instituto de Química, Universidade de São […]Take a Tour
The neuroprotective properties of the superoxide dismutase mimetic tempol correlate with its ability to reduce pathological glutamate release in a rodent model of stroke.
Free Radic Biol Med. 2014 Dec;77:168-82. The neuroprotective properties of the superoxide dismutase mimetic tempol correlate with its ability to reduce pathological glutamate release in a rodent model of stroke. Dohare P1, Hyzinski-García MC1, Vipani A1, Bowens NH1, Nalwalk JW1, Feustel PJ1, Keller RW Jr1, Jourd’heuil D2, Mongin AA3. 1Center for Neuropharmacology and Neuroscience, Albany […]Take a Tour
Circulation. 2015 Jan 20;131(3):289-99. Strategy for identifying repurposed drugs for the treatment of cerebral cavernous malformation. Gibson CC1, Zhu W1, Davis CT1, Bowman-Kirigin JA1, Chan AC1, Ling J1, Walker AE1, Goitre L1, Delle Monache S1, Retta SF1, Shiu YT1, Grossmann AH1, Thomas KR1, Donato AJ1, Lesniewski LA1, Whitehead KJ1, Li DY2. 1From the Program in […]Take a Tour
Low Superoxide Dismutase and Catalase Activities and their Correlation with Malondialdehyde In Schizophrenic Patients
Indian J Clin Biochem. 2004 Jul;19(2):114-8. Superoxide Dismutase and Catalase Activities and their Correlation with Malondialdehyde in Schizophrenic Patients. Rukmini MS1, D’Souza B, D’Souza V. 1Department of Biochemistry, Centre for Basic Sciences, Kasturba Medical College, Bejai, 575 004 Mangalore, India. Abstract Free radical mediated pathological processes may have a role in schizophrenia. Free radicals (oxy […]Take a Tour
A phase I study of topical Tempol for the prevention of alopecia induced by whole brain radiotherapy.
Clin Cancer Res. 2004 Oct 1;10(19):6411-7. A phase I study of topical Tempol for the prevention of alopecia induced by whole brain radiotherapy. Metz JM¹, Smith D, Mick R, Lustig R, Mitchell J, Cherakuri M, Glatstein E, Hahn SM. ¹Department of Radiation Oncology, University of Pennsylvania, Philadelphia Abstract PURPOSE: Complete alopecia is a universal complication […]Take a Tour
Antioxid Redox Signal. 2007 Oct;9(10):1731-43. Forum Review: Therapeutic and clinical applications of nitroxide compounds. Soule BP¹, Hyodo F, Matsumoto K, Simone NL, Cook JA, Krishna MC, Mitchell JB. ¹ Radiation Biology Branch, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland Abstract Nitroxide compounds have been used for many years as biophysical tools, but only […]Take a Tour
Oxidative nucleotide damage and superoxide dismutase expression in the brains of xeroderma pigmentosum group A and Cockayne syndrome.
Brain Dev. 2005 Jan;27(1):34-8. Hayashi M¹, Araki S, Kohyama J, Shioda K, Fukatsu R. Abstract Xeroderma pigmentosum group A (XPA) and Cockayne syndrome (CS) are caused by a genetic defect of nucleotide excision repair mechanisms, showing cutaneous hypersensitivity to sunlight and progressive neurological disturbances. The cause of neurological abnormalities has yet to be clarified and […]Take a Tour
Neuropathology. 2009 Feb;29(1):1-8. Hayashi M¹. ¹Department of Clinical Neuropathology, Tokyo Metropolitan Institute for Neuroscience, Tokyo, Japan. Abstract Oxidative stress is one of the predisposing factors in adult neurological disorders. We have examined the involvement of oxidative stress in child-onset neurodegenerative disorders, and here we review the findings from our analysis. In cases of Cockayne syndrome, […]Take a Tour