2013, Number 1
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Rev Cub Gen 2013; 7 (1)
Alterations in the cellular redox state in cuban patients with autistic spectrum disorders
Carmenates ND, Monzón BG, Lardoeyt FR, Riverón FG, Lemus MG, Martínez BO, Cásido RM, Llamos PA
Language: Spanish
References: 26
Page: 12-17
PDF size: 404.96 Kb.
ABSTRACT
Autism is a behavior disorder with a marked communication and social interaction deficit. In turn, it also constitutes one of the most complex problems from the personal, familial and social points of view that can appear in infancy. It has been suggested that oxidative stress plays a role in the physiopathology that lies behind the emergence of conducts defining autism. The present investigation was carried out with the objective of measuring oxidative damage and antioxidant defense markers in patients with autistic spectrum disorders. A total of 15 cases and 30 controls were studied, determining the oxidative damage and antioxidant defense markers to all of them. Plasmatic level values of malondialdehyde and advanced protein oxidation products turned out to be higher in the cases than in controls. The catalase mean intraerythrocytic activity level was less in the cases (p=0,000003), while no differences were found between the superoxide dismutase mean activity level values in both groups. Free thiols plasmatic concentrations were greater (p=0,020) in patients as compared with controls. Results of this study suggest the presence of oxidative stress conditions in those patients with autistic spectrum disorders. These evidences must be obtained for a greater number of cases due to their possible usefulness in therapeutic strategies.
REFERENCES
American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 4th ed. Washington, DC: American Psychiatric Association; 1994.
Wingate M, Mulvihill B, Kirby RS, Pettygrove S, Cunniff C, Meaney F, et al. Prevalence of Autism Spectrum Disorders-Autism and Developmental Disabilities Monitoring Network. 14 Sites, UnitedStates, 2008. MMWR Surveill Summ. 2012;61(3):1-19.
Hallmayer J, Cleveland S, Torres A, Phillips J, Cohen B, Torigoe T, et al. Genetic heritability and shared environmental factors among twin pairs with autism. Arch Gen Psychiatry. 2011;68(11):1095-102.
Jones DP. Redefining Oxidative Stress. Antioxidants & Redox Signaling. 2006;8:1865-79.
Coleman M. Advances in autism research. Dev Med Child Neurol. 2005;47:148.
Guo Z, Kozlov S, Lavin M, Person MD, Paull TT. ATM Activation by Oxidative Stress. Science. 2010;330(6003):517-21.
Witko SV, Friedlander M, Nguyen KT, Capeillère BC, Thu NA, Zingraff J, et al. Advanced oxidation protein products as a novel marker of oxidative stress in uremia. Kidney International. 1996;49:1304-13.
Marklund S, Marklund G. Involvement of superoxide anion radical in the autoxidation of pyrogallol and a convenient assay for superoxide dismutase. Eur J Biochem. 1974;47:469-74.
Aebi H. Catalase in vitro. Meth Enzymol. 1984;105:121.
Paglia DE, Valentine WN. Studies on the quantitative and qualitative characterization of erythrocyte glutathione peroxidase. J Lab Clin Med. 1967;70:158-169.
Carlberg I, Mannervik B. Glutathione reductase. Meth Enzymol. 1985;113:485-90.
Sedlak J, Lidsay RH. Estimation of total protein bound and non-protein sulfhydryl group in tissue with Ellman’s reagent. Anal. Biochem 1968;25:192-205
Chauhan A, Chauhan V. Oxidative stress in autism. Pathophysiology. 2006;13:171-81.
Kühn H, Borchert A. Regulation of enzymatic lipid peroxidation: the interplay of peroxidizing and peroxide reducing enzymes. Free Radic Biol Med. 2002;33(2):154-72.
Imai H, Nakagawa Y. Biological significance of phospholipid hydroperoxide glutathione peroxidase (PHGPx, GPx4) in mammalian cells. Free Radic Biol Med. 2003;34(2):145-69.
Levraut J, Iwase H, Shao ZH, Vanden Hoek TL, Schumacker T. Cell death during ischemia: relationship to mitochondrial depolarization and ROS generation. Am J Physiol Heart Circ Physiol. 2003;284(2):H549-58.
Stadtman ER, Levine RL. Protein oxidation. Ann N Y Acad Sci. 2000;899:191-208.
Ghezzo A, Visconti P, Abruzzo PM, Bolotta A, Ferreri C, et al. Oxidative Stress and Erythrocyte Membrane Alterations in Children with Autism: Correlation with Clinical Features. PLoS ONE 2013;8(6):e66418
Grune T, Merker K, Sandig G, Davies KJ. Selective degradation of oxidatively modified protein substrates by the proteasome. Biochem Biophys Res Commun. 2003;305(3):709-18.
20. Witko-Sarsat V, Friedlander M, Nguyen-Khoa T, Capeillère-Blandin C, Nguyen AT, Canteloup S, et al. Advanced oxidation protein products as novel mediators of inflammation and monocytes activation in chronic renal failure. J Immunol. 1998;161:2524-2532.
Headlam HA, Davies MJ. Cell-mediated reduction of protein and peptide hydroperoxides to reactive free radicals. Free Radic Biol Med. 2003;34(1):44-55.
Vergani Lauraa, Lanza Cristina, Rivaro Paola, Abelmoschi M. Luisa, Genti Shyti, Veneselli Edvige, Minniti Giuseppe, Grasselli Elena, Canesi Laura, Voci Adriana. Metals, metallothioneins and oxidative stress in blood of autistic children. Research in Autism Spectrum Disorders. 2010.
Geier, Kern, & Geier. A prospective study of oxidative stress biomarkers in autistic disorders. Electronic Journal of Applied Psychology: Innovations in Autism. 2009;5(1):2-10.
Myhrstad MC, Carlsen H, Nordström O, Blomhoff R, Moskaug JØ. Flavonoids increase the intracellular glutathione level by transactivation of the gamma-glutamylcysteine synthetase catalytical subunit promoter. Free Radic Biol Med. 2002;32(5):386-93.
Novo E, Parola M. Redox mechanisms in hepatic chronic wound healing and fibrogenesis. Fibrogenesis Tissue Repair. 2008;1:5.
Castellano-Higuera A, González-Reimers E, Alemán-Valls MR, Abreu-González P, Santolaria-Fernández F, Vega-Prieto de la M, Gómez-Sirvient JL and Pelazas-gonzález R. Cytokines and Lipid Peroxidation in Alcoholics UIT Chronic Hepatitis C Virus Iinfection. Alcohol & Alcoholism. 2008;43(2):137-42.