Oxidative stress after acute and chronic application of β-amyloid fragment 25-35 in cortical cultures

Carla Café, Carla Torri, Laura Bertorelli, Nadia Angeretti, Elisa Lucca, Gianluigi Forloni, Fulvio Marzatico

Research output: Contribution to journalArticlepeer-review


The aim of this work was to investigate whether free radical reactions play a role in β-amyloid neurotoxicity. Rat cortical neurons were exposed acutely (24 h) or chronically (3, 7 days) to β-amyloid biologically active fragment β 25-35 (50 μM). In these conditions, where only the longest exposure induced neuronal death, superoxide dismutase activity was increased after acute exposure but no change was detected after chronic treatments, whereas a different pattern was observed for glutathione peroxidase. In the basal condition, there was an eight-fold increase in dichlorofluoroscein, used as peroxide production marker, in neuronal cells after 7 days treatment with β 25-35. Moreover, the intracellular peroxide production induced by Fe2+/ascorbate stimulation was amplified by β 25-35, increasingly up to 7 days of exposure, by which time the dichlorofluoroscein-stimulated levels were 33 times higher than in controls. In conclusion, our results show that oxidative stress and free radical production are linked to β 25-35 exposure and may contribute to neurodegenerative events associated with β-amyloid deposits in Alzheimer's disease.

Original languageEnglish
Pages (from-to)61-65
Number of pages5
JournalNeuroscience Letters
Issue number1
Publication statusPublished - Jan 12 1996


  • β-Amyloid
  • Alzheimer's disease
  • Free radicals
  • Peroxide production
  • Primary tissue culture

ASJC Scopus subject areas

  • Neuroscience(all)


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