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Panminerva Medica 1999 December;41(4):335-9

lingua: Inglese

Free rad­i­cals: impor­tant ­cause of pathol­o­gies ­refer to age­ing

Venarucci D., Venarucci V., Vallese A., Battilà L., Casado A.*, De La Torre R.* and Encarnation Lopez Fernandes Ma.*

From ­the Center of Clinical Chemistry I.N.R.C.A., Scientific Institute for Hospitalization ­and Therapy, Fermo (Italy)
* Centro De Investigationes Biologicas, Madrid (España)


Free rad­i­cal ­are high­ly reac­tive chem­i­cal spe­cies ­with an ­unpaired elec­tron in an atom­ic or molec­u­lar orbi­tal. In bio­log­i­cal ­systems, ­the ­most impor­tant ­free rad­i­cals ­are super­ox­ide ­anion ­and hydro­gen per­ox­ide; in ­the pres­ence of tran­si­tion met­als ­such as ­iron, cop­per ­and man­ga­nese ­both ­these ­free rad­i­cals pro­duce hydrox­yl rad­i­cals. Free rad­i­cals ­attack pro­teins, ­nuclei ­acids ­and mem­branes con­tain­ing ­large quan­tities of poly­un­sat­u­rat­ed fat­ty ­acids. Because of ­their tox­ic­ity, ­the organ­ism ­has devel­oped ­ways to deac­ti­vate ­them. The super­ox­ide dis­mu­tase ­enzyme (SOD) cat­a­lyz­es dis­mu­ta­tion of ­the super­ox­ide rad­i­cal ­into hydro­gen per­ox­ide ­and oxy­gen hydro­gen per­ox­ide is in ­turn ­reduced to ­water ­and oxy­gen by per­ox­i­dase glu­tath­i­one ­and cat­a­lase ­enzymes. The pro­duc­tion of rad­i­cals in ­the ­brain is ­due to cat­e­chol­a­mine metab­olism ­such as dop­a­mine ­and nor­epi­neph­rine ­and is ­increased by ­the pres­ence of tran­si­tion met­als ­and by a defi­cien­cy of anti­ox­i­dant ­agents ­such as vita­min E. Two ­main ­groups of demen­tia ­exist in old­er ­age: ­the mul­ti-infarc­tu­al demen­tias, ­caused by cereb­ro­vas­cu­lar dis­or­ders ­and ­the pri­mary degen­er­a­tive dis­or­ders ­such as Alzheimer, ­where no vas­cu­lar dis­ease is evi­dent. Free rad­i­cals ­play an impor­tant ­role in Parkinson’s dis­ease, in Alzheimer’s dis­ease ­and in ­stroke. The val­ue of ­SOD ­and ­CAT activ­ity fol­low­ing ­the ­above men­tioned degen­er­a­tive dis­eas­es dif­fer ­among ­the var­i­ous stud­ies car­ried ­out. In Alzheimer’s dis­ease, ­the val­ue of ­SOD activ­ity prob­ably increas­es in ­the neu­ro­path­o­log­i­cal­ly ­involved are­as. In ­stroke, ­the ­SOD val­ue ­does ­not ­vary ­either in ­the ischem­ic ­area or in ­the ­peri-infarc­tu­al ­one dur­ing ­the ­first 24 ­hrs ­after ­lesion, ­while ­the ­CAT val­ue decreas­es.

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