covid
Buscar en
Gaceta Médica de Bilbao
Toda la web
Inicio Gaceta Médica de Bilbao Importancia de las especies reactivas al oxigeno (radicales libres) y los antiox...
Journal Information
Vol. 106. Issue 3.
Pages 106-113 (January 2009)
Share
Share
Download PDF
More article options
Vol. 106. Issue 3.
Pages 106-113 (January 2009)
Full text access
Importancia de las especies reactivas al oxigeno (radicales libres) y los antioxidantes en clinica.
The importance of reactive oxygen species (free radicals) and antioxidants in clinic
Oxigeno espezie erreaktiboek (erradikal libreak) eta antioxidatzaileek klinikan duten garrantzia
Visits
24254
A. San-Miguel
Corresponding author
asanmiguel@hurh.sacyl.es

Correspondencia: Dr. A. San-Miguel. Servicio de Análisis Clínicos., Hospital Universitario Rio Hortega., Rondilla de Santa Teresa 9., 47001. Valladolid. Castilla y León. Espa˜a UE.
, F.J. Martin-Gil
Servicio de Análisis Clínicos. Hospital Universitario Rio Hortega. Valladolid. Castilla y León. Espa˜a UE.
This item has received
Article information
Resumen

Las reacciones de óxido reducción tienen una amplia distribución en la naturaleza, y las células de nuestro organismo no están ajenas a estos procesos; muy por el contrario la transformación de los alimentos en sustratos más simples, de los cuales es posible obtener energía, involucra reacciones químicas de óxido reducción. Durante el proceso de respiración celular se consume oxígeno, y se genera ATP (adenosin trifosfato), quedando como productos dióxido de carbono y agua. Sin embargo, durante esta normal transformación se producen también otras moléculas residuales, las especies reactivas del oxígeno o radicales libres.

Los radicales libres (RL) son átomos o moléculas inestables, altamente reactivas que atacan los enlaces de proteínas de los tejidos, los fosfolípidos poliinsaturados de las membranas celulares, carbohidratos, y los ácidos nucleicos de las células. Al actuar, se activa una reacción en cadena que podría incluso llevar a la muerte de la célula. La producción de radicales libre es un fenómeno natural, dinámico y continuo, el da˜o que estos compuestos puedan provocar depende de un delicado equilibrio con los sistemas antioxidantes que protegen a las células de nuestro organismo. Los mecanismos de defensa para neutralizar a los radicales libres son múltiples y variados y pueden dividirse en dos grupos.

El estrés oxidativo se produce al romperse el equilibrio entre la producción de especies reactivas del oxígeno y los mecanismos de defensa antioxidante, lo que lleva a una variedad de cambios fisiológicos y bioquímicos que provocan el deterioro y muerte celular. Este tipo de da˜o puede ser medido mediante métodos directos e indirectos.

Palabras clave:
Estrés oxidativo
especies reactivas al oxígeno
antioxidantes
Summary

Oxide reduction reactions are well spread out in nature, and the cells of our organism are not so far away from these processes; on the contrary, the transformation of foods into more single strata, from which it is possible to obtain energy, involves chemical oxide reduction reactions. Oxygen is consumed during the cellular respiration process and ATP (adenosine triphosphate) is generated, ending up as carbon dioxide and water products. However, other residual molecules, reactive oxygen species or free radicals are also produced in the course of this normal transformation. Free radicals (FR) are unstable atoms or molecules which are highly reactive and attack the links maintained by proteins with tissues, polyunsaturated phospholipids of cellular membranes, carbohydrates and nucleic acids in cells. When they act, a chain reaction is triggered off that can even lead to the death of the cell. The production of free radicals is a natural, dynamic and continuous phenomenon; the damage these compounds can cause depends on a delicate balance with the antioxidant systems that protects the cells of our organism. There are many different defence mechanisms available for neutralising free radicals, and these can be divided into two groups. Oxidative stress occurs when the balance between the production of reactive oxygen species and antioxidant defence mechanisms is broken, which leads to a variety of physiological and biochemical changes that in turn cause damage and cellular death. This type of damage can be measured using both direct and indirect methods.

Key words:
oxidative stress
reactive oxygen species
antioxidants
Laburpena

Erredukziozko oxido erreakzioak naturan oso barreiatuta daude, eta gure organismoko zelulek ere ezin diete ihes egin prozesu horiei. Bestalde, elikagaiak substratu sinpleagoetan eraldatzeak (horietatik energia eskuratzeko) erredukziozko oxido erreakzio kimikoak eragiten ditu. Arnasketa zelularra prozesuan, oxigenoa kontsumitu eta ATP (adenosin trifosfatoa) sortzen da; beraz, karbono dioxidoa eta ura geratzen zaizkigu produktu moduan. Alabaina, eraldaketa arrunt honetan, bestelako hondakin molekula batzuk ere sortzen dira: oxigeno espezie erreaktiboak edo erradikal libreak, alegia. Erradikal Libreak (EL) atomo edo molekula ezegonkorrak dira, oso-oso erreaktiboak, eta ehunen proteina loturei, zelula mintzen fosfolipido poliinsaturatuei, karbohidratoei eta zelulen azido nukleikoei erasotzen diete. Lanean hastean, kate erreakzioa aktibatzen da, eta zelula hiltzera ere irits liteke. Erradikal libreen produkzioa gertakari natural, dinamiko eta etengabekoa da; konposatu horiek eragin dezaketen kaltea, ordea, gure organismoko zelulak babesten dituzten antioxidatzaile sistemekiko oreka zail baten araberakoa izango da. Ezin konta ahala defentsa modu daude erradikal libreak neutralizatzeko; askotarikoak dira gainera, eta bi multzotan bana daitezke. Oxidazio estresa, hain zuzen, oxigeno espezie erreaktiboen produkzioaren eta defentsa modu antioxidatzaileen arteko oreka hausten denean gertatzen da. Horrek aldaketa fisiologiko eta biokimiko ugari dakartza, eta ondorioz, zelula hondatzea eta baita hiltzea ere gerta liteke. Era honetako kalteak metodo zuzen eta zeharkakoekin neur daitezke.

Hitz gakoak:
oxidazio estresa
oxigeno espezie erreaktiboak
antioxidatzaileak
Full text is only aviable in PDF
Bibliografia
[1.]
Halliwell B, Gutteridge JMC. (2000) Free radicáis in biology and medicine (3rd. ed.).
[2.]
Hageman J.J., Bast A., Vermeulen V.B..
Monitoring of oxidative free radical damage in vivo analytical aspects.
Chem. Biol. Interactions, 82 (1992), pp. 243-293
[3.]
Lachance P.A., Nakat Z., Jeong W..
Antioxidants: an integrative approach.
Nutrition, 17 (2001), pp. 835-838
[4.]
Davies K.J.A..
Oxidative stress: The paradox of aerobio life.
Biochem Soc Symp., 61 (1995), pp. 1-31
[5.]
Borja G..
Los radicales libres mitocondriales como factores principales determinantes de la velocidad de envejecimiento.
Rev Esp Geront Geriatr., 31 (1996), pp. 153-161
[6.]
McCord J.M., Fridovich I..
Superoxide Dismutase: an enzymic function for erythrocuprein (hemocuprein).
J. Biol. Chem., 244 (1969), pp. 6049-6055
[7.]
Reed D.J., Fariss M.W..
Gluíaíhione Depleíion and suscepíibility.
Pharmacol Revi., 2 (1984), pp. 255-335
[8.]
Harris E.D..
Regulation of antioxidant enzymes.
FASEB J., 6 (1992), pp. 2675-2683
[9.]
Céspedes T., Sanchez D..
Algunos aspectos sobre el estrés oxidativo, el estado antioxidante y la terapia de suplementación.
RevCubana Cardiol., 14 (2000), pp. 55-60
[10.]
Dhremer E., Valls V., Muñiz P., Cabo J., Sáez G.T..
8-Hydroxydeoxyguanosine and antioxidant status in rat liver fed with olive and corn oil diets. Effect of ascorbic acid supplementation.
J Food Lipids, 8 (2001), pp. 281-294
[11.]
Borja G..
Ascorbic acid and aging.
Ascorbic Add: Biochemistry and Biomedicaí Cell Biology, pp. 157-188
[12.]
Blot W.J., Li J.Y., Taylor P.R., et al.
Nutrition intervention triáis in Linxian, China: supplementation with specified vitamin/mineral combinations, cáncer incidence, and disease-specified mortality in the general.
Nat. Cáncer, 85 (1993), pp. 1483-1491
[13.]
Gey K.F., Moser U.K., Jordán P., Stahelin H.B., Eichholzer M., Luedin E..
Increased risk of cardiovascular disease at suboptimal plasma concentrations of essential antioxidants: an epidemíological update with special attention to carotene and vitamin C.
Am J Clin Nutr., 57 (1993), pp. 787S-797S
[14.]
Vítale West S., Hallfrisch J., Alston C., Wang F., Moorman C., Muller D., Singh Vy Taylor H.R..
Plasma antioxidants and risk of cortical and nuclear cataract.
Epidemiol., 4 (1993), pp. 195-203
[15.]
Chen K., Suh J., Carr A.C., Morrow J.D., Zeind J., Frei B..
Vitamin C suppresses oxidative lipid damage in vivo, even in the presence of iron overload.
Am. J. Physiol. Endocrin. Metab., 279 (1993), pp. E1406-E1412
[16.]
Ames B.N., Signage M.K..
Oxidants are a major contributor to cancer and aging. En: DNA and Free radicals.
Ellis Horwood, Chinchester, England,, (1993), pp. 1-15
[17.]
Cao G., Sofíc E., Prior R.L..
Antioxidant and prooxidant behavior of flavonoids: Structure-activity relationships.
Free Radic. Biol. Med., 22 (1997), pp. 749-760
[18.]
Sies H., Stahl W., Sundquist A.R..
Antioxidant functions of vitamins.
Annals of the New York Academy of Sciences, 669 (1992), pp. 7-20
[19.]
Herrera B., Alvarez A.M., Sánchez A..
Active oxygen species medíate the mitochondrial-dependent apoptosis induced by transforming growth factor in fetal hepatocytes.
FASEB J., 115 (2001), pp. 741-749
[20.]
Levine R.L., Garland Oliver C.N., Amici A., Climent I., Lenz A.G., Ahn B.W., Shaltiel S., Stadman E.R..
Determination of carbonyl content in oxidatively modified proteins.
Methods Enzymol., 186 (1990), pp. 464-478
[21.]
Halliwell B., Aruoma O.I..
DNA damage by oxygen derived species.
FEBS Letter, 281 (1991), pp. 9-19
[22.]
Muñiz P., Valls V., Perez-Broxeta C., Iradi A., Climent J.V., Oliva M., Saez G.T..
The role of 8-hydroxy-2'deoxyguanosine in Rifamycininduced DNA damage.
Free Radic. Biol. Med., 18 (1995), pp. 747-755
[23.]
Halliwell B..
Vitamin C and genomic stability.
Mutation ReseArch., 475 (2001), pp. 29-35
[24.]
Ames B.N., Signage M.K..
Oxidants are a major contributor to cáncer and aging.
DNA and Free Radicals, Ellis Horwood, (1993),
[25.]
Borja G..
Los radicales libres mitocondriales como factores principales determinan¬tes de la velocidad del envejecimiento.
Rev. Esp. Geront. Geriatr., 31 (1996), pp. 153-161
[26.]
Ajmani R.S., et al.
Oxidative stress and hemorheological changes induced by acute treadmill exercise.
Clin Hemorheol Microcirc, 28 (2003), pp. 29-40
[27.]
Chevion S., et al.
Plasma antioxidant status and cell injury after severe physical exercise.
Proc Natl Acad Sci U S A, 100 (2003), pp. 5119-5123
[28.]
Cooper E.C., et al.
Exercise, free radicals and oxidative stress.
Biochem Soc Trans., 30 (2002), pp. 280-285
[29.]
Dillard C.J., et al.
Effects of exercise, vitamin E, and ozone on pulmonary function and lipid peroxidation.
J.Appl.Physiol., 45 (1978), pp. 927-932
[30.]
Evans W.J..
Vitamin E, vitamin C, and exercise.
Am J Clin Nutr., 72 (2000), pp. 647S-6452S
[31.]
De Oliveira S.L., et al.
Carbohydrate-energy restriction may protect the rat brain against oxidative damage and improve physical performance.
Br J Nutr., 89 (2003), pp. 89-96
[32.]
Finkel T., Holbrook N..
Oxidants, oxidative stress and the biology of ageing.
Nature, 408 (2000), pp. 239-247
[33.]
Groussard C., et al.
Physical fitness and plasma non-enzymatic antioxidant status at rest and after a wingate test.
Can J Appl Physiol., 28 (2003), pp. 79-92
[34.]
Henriksen E.J., Saengsirisuwan V..
Exercise training and antioxidants:relief from oxidative stress and insulin resistance.
Exerc Sport Sci Rev., 31 (2003), pp. 79-84
[35.]
Sacheck J.M., Blumberg J.B..
Role of vitamin E and oxidative stress in exercise.
Nutrition, 17 (2001), pp. 809-814
[36.]
Hoppeler H., Vogt M..
Muscle tissue adaptations to hypoxia.
J Exp Biol., 204 (2001), pp. 3133-3139
[37.]
Johnson P..
Antioxidant enzyme expression in health and disease: effects of exercise and hypertension.
Comp Biochem Physiol C Toxicol Pharmacol., 133 (2002), pp. 493-505
[38.]
Ji L.L..
Exercise-induced modulation of antioxidant defense.
Ann N Y Acad Sci., 959 (2002), pp. 82-92
[39.]
Powers S., Lennon S..
Analysis of cellular responses to free radicals: focus on exercise and skeletal muscle.
Proceed Nutr Soc., 58 (1999), pp. 1025-1033
[40.]
Vassilakopoulos T., et al.
Antioxidants attenuate the plasma cytokine response to exercise in humans.
J Appl Physiol., 94 (2003), pp. 1025-1032
[41.]
Sen C.K..
Antioxidants in exercise nutrition.
Sports Med., 31 (2001), pp. 891-908
Copyright © 2009. Academia de Ciencias Médicas de Bilbao
Download PDF
Article options