ABSTRACT
Excitotoxicity elicited by overactivation of N-methyl-D-aspartate receptors is a well-known characteristic of quinolinic acid-induced neurotoxicity. However, since many experimental evidences suggest that the actions of quinolinic acid also involve reactive oxygen species formation and oxidative stress as major features of its pattern of toxicity, the use of antioxidants as experimental tools against the deleterious effects evoked by this neurotoxin becomes more relevant. In this work, we investigated the effect of a garlic-derived compound and well-characterized free radical scavenger, S-allylcysteine, on quinolinic acid-induced striatal neurotoxicity and oxidative damage. For this purpose, rats were administered S-allylcysteine (150, 300 or 450 mg/kg, i.p.) 30 min before a single striatal infusion of 1 microl of quinolinic acid (240 nmol). The lower dose (150 mg/kg) of S-allylcysteine resulted effective to prevent only the quinolinate-induced lipid peroxidation (P < 0.05), whereas the systemic administration of 300 mg/kg of this compound to rats decreased effectively the quinolinic acid-induced oxidative injury measured as striatal reactive oxygen species formation (P < 0.01) and lipid peroxidation (P < 0.05). S-Allylcysteine (300 mg/kg) also prevented the striatal decrease of copper/zinc-superoxide dismutase activity (P < 0.05) produced by quinolinate. In addition, S-allylcysteine, at the same dose tested, was able to reduce the quinolinic acid-induced neurotoxicity evaluated as circling behavior (P < 0.01) and striatal morphologic alterations. In summary, S-allylcysteine ameliorates the in vivo quinolinate striatal toxicity by a mechanism related to its ability to: (a) scavenge free radicals; (b) decrease oxidative stress; and (c) preserve the striatal activity of Cu,Zn-superoxide dismutase (Cu,Zn-SOD). This antioxidant effect seems to be responsible for the preservation of the morphological and functional integrity of the striatum.
Subject(s)
Antioxidants/pharmacology , Cysteine/analogs & derivatives , Cysteine/pharmacology , Garlic/chemistry , Neurotoxicity Syndromes/prevention & control , Oxidative Stress/drug effects , Quinolinic Acid/antagonists & inhibitors , Quinolinic Acid/toxicity , Animals , Behavior, Animal/drug effects , Blotting, Western , Body Weight , Glutathione Peroxidase/metabolism , Lipid Peroxidation/drug effects , Male , Neostriatum/drug effects , Neostriatum/enzymology , RNA, Messenger/biosynthesis , RNA, Messenger/genetics , Rats , Rats, Wistar , Reactive Oxygen Species/metabolism , Reverse Transcriptase Polymerase Chain Reaction , Superoxide Dismutase/metabolismABSTRACT
The effects of S-allylcysteine on oxidative damage and spatial learning and memory deficits produced by an intrahippocampal injection of amyloid-beta peptide 25-35 (Abeta(25-35)) in rats were investigated. The formation of reactive oxygen species, lipid peroxidation and the activities of the antioxidant enzymes superoxide dismutase and glutathione peroxidase were all measured in hippocampus 120 min after Abeta(25-35) injection (1 microl of 100 microM solution), while learning and memory skills were evaluated 2 and 35 days after the infusion of Abeta(25-35) to rats, respectively. Abeta(25-35) increased both reactive oxygen species and lipid peroxidation, whereas pretreatment with S-allylcysteine (300 mg/kg, i.p.) 30 min before peptide injection decreased both of these markers. In addition, Abeta(25-35)-induced incorrect learning responses were prevented in most of trials by S-allylcysteine. In contrast, enzyme activities were found unchanged in all groups tested. Findings of this work: (i) support the participation of reactive oxygen species in Abeta(25-35)-induced hippocampal toxicity and learning deficits; and (ii) suggest that the protective effects of S-allylcysteine were related to its ability to scavenge reactive oxygen species.
Subject(s)
Amyloid beta-Peptides/adverse effects , Cysteine/analogs & derivatives , Cysteine/therapeutic use , Hippocampus/drug effects , Hippocampus/metabolism , Oxidative Stress/drug effects , Amyloid beta-Peptides/administration & dosage , Animals , Cysteine/administration & dosage , Cysteine/chemical synthesis , Drug Administration Schedule , Fluoresceins , Garlic/chemistry , Glutathione Peroxidase/chemistry , Glutathione Peroxidase/metabolism , Hippocampus/physiopathology , Injections, Intraperitoneal , Learning Disabilities/chemically induced , Learning Disabilities/prevention & control , Lipid Peroxidation/drug effects , Lipid Peroxidation/physiology , Male , Maze Learning/drug effects , Maze Learning/physiology , Memory/drug effects , Rats , Rats, Wistar , Reactive Oxygen Species/antagonists & inhibitors , Reactive Oxygen Species/chemistry , Reactive Oxygen Species/metabolism , Spatial Behavior/drug effects , Spatial Behavior/physiology , Superoxide Dismutase/chemistry , Superoxide Dismutase/metabolismABSTRACT
Se presentan los resultados obtenidos en la determinación de anticuerpos totales para citomegalovirus en sangre procedentes de donantes. Se encontró una alta positividad (65 %) que concuerda con lo comunicado en la literatura. Se sugiere realizar esta determinación a la sangre que se va a utilizar en inmunosuprimidos, embarazadas, recién nacidos prematuros y receptores de órganos, cuando no sea posible realizarlo a todas las donaciones
Subject(s)
Cytomegalovirus , Antibodies/blood , Blood DonorsABSTRACT
Se presentan los resultados obtenidos en la determinación de anticuerpos totales para citomegalovirus en sangre procedentes de donantes. Se encontró una alta positividad (65 %) que concuerda con lo comunicado en la literatura. Se sugiere realizar esta determinación a la sangre que se va a utilizar en inmunosuprimidos, embarazadas, recién nacidos prematuros y receptores de órganos, cuando no sea posible realizarlo a todas las donaciones
