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
Oxidative stress in developmental brain disorders.
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
Possible protective effect by SOD on UV damage in xeroderma pigmentosum (XP)
J Invest Dermatol. 1989 Oct;93(4):506-10. Reduced superoxide dismutase activity in xeroderma pigmentosum fibroblasts. Nishigori C¹, Miyachi Y, Imamura S, Takebe H. ¹Department of Dermatology, Faculty of Medicine, Kyoto University, Japan. Abstract This study was performed in order to assess the possible protective effect of superoxide dismutase (SOD) on ultraviolet (UV) damage in xeroderma pigmentosum […]Take a Tour
New Treatment Method to Help Women Suffering From Fibrocystic Disease
FOR IMMEDIATE RELEASE August 19, 2014 Fibrocystic disease may affect up to 50 percent of all women (INDIANAPOLIS, Ind.) –A new patent has been issued for a method that uses the SOD-mimetic agent TEMPOL to treat fibrocystic disease of the breast (FD). Approximately 20 percent of women suffering from FD, which is more commonly known […]Take a Tour
Cancer chemoprevention by the antioxidant tempol acts partially via the p53 tumor suppressor.
Hum Mol Genet. 2005 Jun 15;14(12):1699-708. Epub 2005 May 11. Erker L¹, Schubert R, Yakushiji H, Barlow C, Larson D, Mitchell JB, Wynshaw-Boris A. ¹Department of Pediatrics, UCSD School of Medicine, La Jolla, CA Abstract We previously demonstrated that the nitroxide antioxidant tempol (4-hydroxy-2,2,6,6-tetramethylpiperidine-N-oxyl) increased latency to tumorigenesis and doubled (100%) the lifespan of Atm-deficient […]Take a Tour
Neuroprotective effects of TEMPOL in central and peripheral nervous system models of Parkinson’s disease.
Biochem Pharmacol. 2005 Nov 1;70(9):1371-81. Liang Q¹, Smith AD, Pan S, Tyurin VA, Kagan VE, Hastings TG, Schor NF. ¹Department of Pediatrics, University of Pittsburgh, Pittsburgh, PA Abstract TEMPOL (4-hydroxy-2,2,6,6-tetramethylpiperidine-N-oxyl) is a stable nitroxyl antioxidant. Previous studies have suggested that TEMPOL is protective in acute disorders thought to involve reactive oxygen species (ROS), such as […]Take a Tour
Nitroxide stable radical suppresses autoimmune uveitis in rats.
Free Radic Biol Med. 1999 Jul;27(1-2):7-15. Zamir E¹, Zhang R, Samuni A, Kogan M, Pe’er J. ¹Department of Ophthalmology, Hadassah-Hebrew University Medical School, Jerusalem, Israel. Abstract Free radicals have been implicated in the pathogenesis of experimental autoimmune uveoretinitis (EAU). Nitroxides are stable radicals with a superoxide-dismutase-mimicking activity, which exert an anti-inflammatory effect in various animal […]Take a Tour
Tempol Moderately Extends Survival in a hSOD1G93A ALS Rat Model by Inhibiting Neuronal Cell Loss, Oxidative Damage and Levels of Non-Native hSOD1G93A Forms
PLoS One. 2013; 8(2): e55868. Linares E¹, Seixas LV, dos Prazeres JN, Ladd FV, Ladd AA, Coppi AA, Augusto O. ¹Departamento de Bioquímica, Instituto de Química, Universidade de São Paulo, São Paulo, Brazil. Abstract Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by the progressive dysfunction and death of motor neurons by mechanisms […]Take a Tour
Mitochondria-targeted antioxidants for treatment of Parkinson’s disease: Preclinical and clinical outcomes.
Biochimica et Biophysica Acta (BBA) – Molecular Basis of Disease Volume 1842, Issue 8, August 2014, pp 1282–1294 Misfolded Proteins, Mitochondrial Dysfunction, and Neurodegenerative Diseases Jin H1, Kanthasamy A, Ghosh A, Anantharam V, Kalyanaraman B, Kanthasamy AG 1 Parkinson’s Disorder Research Laboratory, Iowa Center for Advanced Neurotoxicology, Department of Biomedical Sciences, Iowa State University, Ames, IA […]Take a Tour