Efecto del ácido alfa lipoico sobre el daño oxidativo inducido por cadmio en corazón, cerebro, riñón, hígado y pulmón de ratas

Autores/as

  • R PRABHU Pharmacy Department, Faculty of Technology and Engineering, The Maharaja Sayajirao University of Baroda-390 001, Gujarat, INDIA.
  • A UPAGANLAWAR Pharmacy Department, Faculty of Technology and Engineering, The Maharaja Sayajirao University of Baroda-390 001, Gujarat, INDIA.
  • R BALARAMAN Pharmacy Department, Faculty of Technology and Engineering, The Maharaja Sayajirao University of Baroda-390 001, Gujarat, INDIA.

Palabras clave:

Ácido alfa lipoico, Antioxidante, Cadmio, Peroxidación lipídica

Resumen

En el presente estudio se investigó el efecto protector del ácido alfa lipoico (ALA) sobre el daño oxidativo inducidopor el cadmio en ratas. El cadmio (100 ppm) suministrado a ratas normales dio lugar a un aumento signifi cativode los niveles de transaminasa glutámico-oxalacética sérica (SGOT), transaminasa glutámico-pirúvica sérica (SGPT)y fosfatasa alcalina (ALP). En los animales expuestos al cadmio se observó igualmente un aumento signifi cativodel nivel de peroxidación lipídica (LPO) y una disminución de los niveles de glutatión reducido (GSH), superóxidodismutasa (SOD), catalasa (CAT) y ATPasas de la membrana (Na+K+-ATPasa, Ca2+-ATPasa y Mg2+-ATPasa) encerebro, pulmón, riñón, hígado y corazón en comparación con el grupo de control. La administración conjunta deALA (25mg/kg/día, i.p.) y cadmio durante treinta días dio lugar a una disminución signifi cativa de los niveles deSGOT, SGPT y fosfatasa alcalina en suero hasta niveles cercanos a los normales. El uso de ALA también supusouna reducción del nivel de MDA y un aumento de los niveles de SOD, CAT, GSH y ATPasas unidas a la membranaen todos los órganos de los animales tratados con cadmio hasta niveles cercanos a los normales. El presente estudiodemuestra el daño inducido por radicales libres derivados de la administración de cadmio sobre distintos órganosy el efecto antioxidante del ALA que protege a los órganos frente a este daño cuando se administra conjuntamentecon cadmio.

Descargas

Los datos de descargas todavía no están disponibles.

Citas

Fulkerson W and Goeller HE .Cadmium: The Dissipated Element. Oak Ridge National Laboratory, Oak Ridge, Tenn., 1973.

Friberg L. Cadmium in the Environment.2nd ed.CRC Press, Cleveland, 1974.

Bryce-Smith S and Stephens R. Exposure to lead. Lancet, 1981:307: 877.

Friberg L, Nordberg GF and Vouk VB. Handbook on the toxicology of metals,1979 : 451-500. Elsevier Biomed Press, New York.

Klos A. Lead, cadmium and mercury content in meals planned for consumption in selected kindergartens in Warsaw. IV International Scientifi c & -Technical Conference, Warsaw 2001:4-5X.

Perry HM, Jr, et al. Variation in the concentration of cadmium in human kidney as a function of age and geographic origin. J. Chronic Dis, 1961: 14: 259.

Ryan PB, Huet N, Maclntosh DL. Longitudinal investigation of exposure to arsenic, cadmium and lead in drinking water. Environ Health Perspect, 2000. 108:731-5.

Yiin SJ, Chern CL, Sheu JY, Tseng WC, Lin TH. Cadmium induced renal lipid peroxidation in rats and protection by selenium Toxicol Environ Health A.; 1999.57:403-13.

Schroeder HA and Balassa JJ. Abnormal trace metals in man: cadmium. J. Chronic Dis.1961.14:236.

Friberg L, Piscator M and Nordberg. Cadmium in the environment.CRC Press, Cleveland, Ohio.1971.

Balaraman, R. Some Pharmacological Investigations of Cadmium.Ph.D. Thesis, M.S.University of Baroda.1986.

Butler EA and Flynn FV. The proteinuria of renal tubular disorders. Lancet, 1958: 2: 978.

Stohs SJ, Bagchi D. Oxidative mechanisms in toxicity of metal ions. Free Radic. Biol. Med, 1995: 18(2): 321-336.

Busse E, Zimmer G, Schopohl B, Kornhuber B. Infl uence of alpha-lipoic acid on intracellular glutathione in vitro and in vivo.Arzneimittelforschung 1992;42:829-831.

Kagan V, Serbinova E, Packer L.Antioxidant effects of ubiquinones in microsomes and mitochondria are mediated by tocopherol recycling. Biochem Biophys. Res. Commun. 1990; 169:851-857.

Slater TF and Sawyer BC. The stimulatory effect of carbon tetrachloride and other halogenoalkanes on peroxidative reactions in rat liver fractions in vitro. Biochem. J, 1971:123:805-814.

Misra HP and Firidovich I. The role of superoxide anion in the auto oxidation of epinephrine and simple assay of superoxide dismutase. J.Biol.chem, 1972:247: 3170-3175.

Sinha AK. Colorimetric assay of catalase.Anal.Biochem,1972: 47:389-394.

Moran MS, Depirre JW and Mannaervik B. Levels of glutathione, glutathione reductase and glutathione-s-transferase activity in rat lung and liver. Biochem. Biophys. Acta, 1979: 582: 67-78.

Bonting SL. Presence of enzyme system in mammalian tissue.In: Bilter, E.E.editor, Membrane and ion transport, 1970: 257-263. Wiley Inter Science, London.

Hjerken S and Pan H. Purifi cation and characterization of two forms of low affi nity calcium ion ATPase from erythrocyte

membranes. Biochem. Biophys. Acta, 1983: 728: 281-288.

Ohinishi T, Suzuki T, Suzuki, Y and Ozawa KAA. Comparative study of plasma membrane magnesium ion ATPase activities in normal regenerating and malignant cells. Biochem. Biophys. Acta,1982: 684:67-74.

Muller L. Protective effects of DL-Lipoic acid on cadmium-induced deterioration of rat hepatocytes. Toxicology 1989; 58:175-185.

Armario A, Compmany L, Borras M and Hidalgo J, Vitamin E supplemented diet reduce lipid peroxidation but do not alter either pituitary-adrenal, glucose and lactate responses to immobilization stress or gastric ulceration, Free Radic Res Commun,1990: 9(2):113.

Sherman M, Antioxidant decade, Pharmacy times, 2000: 66(2):69.

Pappas, Jr. Source of increased aspartate and alanine amino transferase cyclohexidine effect on CCL4 hepatotoxicity. Clinica. Chemica. Acta, 1986:154:181-190.

Othman AI, Misery EL, MA. Role of selenium against lead toxicity in male rats.J.Biochem.Mol.Toxicol,1998: 12(6): 345-349.

Orrenius S and Moldeus P. The multiple role of glutathione in drug metabolism.Trends Pharmac Sci,1984: 5:432.

Meister, A. New aspects of glutathione biochemistry and transport-selective alteration of glutathione metabolism. Nutr. Rev,1984: 42:397.

Karmarkar R, Banik S, Bandyopadhyay S, Chatterjee M. Cadmium induced alteration of hepatic lipid peroxidation, glutathione levels and their possible correlation with chromosomal aberration in mice: a time course study.Mutant. Res.,1998: 397(2):183-190.

Brawn K and Fridovich I. Superoxide radical and superoxide dismutase: threat and defense.Acta Physiol Scand Suppl, 1980: 492: 9-18.

Brenner S and Alison AL. Catalase inhibition: A possible mechanism for the production of Heinz bodies in erythrocytes. Experimentia,1953. 9: 381.

Mam Eation, J.W. (1990).Is Catalase really important? Free radi. Biol. Med. 9,132.

Ayaz SA, Bhandari U, Pillai KK, Infl uence of DL a-lipoic acid and vitamin-E against doxorubicin-induced biochemical and histological changes in the cardiac tissue of rats. Ind J Pharmacol. 2005:37:294-299.

Scholich H, Murphy ME, Sies H. Antioxidant activity of dihydrolipoate against microsomal lipid peroxidation and its

dependence on alpha-tocopherol. Biochem Biophys Acta1989;1001:256-261.

Gubdjorson S, Hallgrimson J, Skuldottir G. Properties of transport adenosine triphosphatase.In: Peter, H., Gresham, G.A., Paoetti, R.Arterial Pollution. New York. Plenum Publishing Corp. 1983:101.

Tanaka R and Strickland KP. Role of Phospholipid in the activation of Na+-K+-ATPase adenosine triphosphatase in beef brain. Arch. Biochem. Biophys., 1965.111, 583-592.

Descargas

Publicado

2008-12-20

Cómo citar

1.
PRABHU R, UPAGANLAWAR A, BALARAMAN R. Efecto del ácido alfa lipoico sobre el daño oxidativo inducido por cadmio en corazón, cerebro, riñón, hígado y pulmón de ratas. Ars Pharm [Internet]. 20 de diciembre de 2008 [citado 19 de abril de 2024];49(4):293-307. Disponible en: https://revistaseug.ugr.es/index.php/ars/article/view/4968

Número

Sección

Artículos Originales