S-Allylcysteine prevents amyloid-β peptide-induced oxidative stress in rat hippocampus and ameliorates learning deficits

Francisca Pérez-Severiano, Raquel Salvatierra-Sánchez, Mayra Rodríguez-Pérez, Elvis Y. Cuevas-Martínez, Jorge Guevara, Daniel Limón, Perla D. Maldonado, Omar N. Medina-Campos, José Pedraza-Chaverrí, Abel Santamaría

Research output: Contribution to journalArticlepeer-review


The effects of S-allylcysteine on oxidative damage and spatial learning and memory deficits produced by an intrahippocampal injection of amyloid-β peptide 25-35 (Aβ(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 Aβ(25-35) injection (1 μl of 100 μM solution), while learning and memory skills were evaluated 2 and 35 days after the infusion of Aβ(25-35) to rats, respectively. Aβ(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, Aβ(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 Aβ(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.

Original languageEnglish (US)
Pages (from-to)197-202
Number of pages6
JournalEuropean Journal of Pharmacology
Issue number3
StatePublished - Apr 12 2004
Externally publishedYes


  • Alzheimer disease
  • Amyloid-β peptide
  • Antioxidant defense
  • Garlic compound
  • Learning
  • Memory
  • Oxidative injury

ASJC Scopus subject areas

  • Pharmacology


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