(-) deprenyl attenuates aluminium induced neurotoxicity in primary cortical cultures

Neurodegeneration. 1996 Jun;5(2):161-7. doi: 10.1006/neur.1996.0023.

Abstract

The role of (-) deprenyl in offering neuroprotection to cortical neurons exposed to Aluminium chloride (AlCl3) was examined. Primary cortical cultures derived from newborn rats were exposed to AlCl3 on 6th day in vitro, at 100,200,400,600,800 and 1000 microM concentrations of AlCl3. After 48 h of AlCl3 exposure, many nerve cell bodies were swollen; a beading of neurites and a disruption of the neuritic network were also observed suggesting neurodegeneration. Lactate dehydrogenase (LDH) efflux increased in a dose-dependent manner (59-120%). (-) Deprenyl co-exposure at concentrations of 10(-7), 10(-8) and 10(-9) M significantly attenuated both the morphological alterations and the LDH efflux induced by AlCl3. This in vitro study has demonstrated that (-) deprenyl can protect neurons from aluminium induced neurotoxicity.

MeSH terms

  • Aluminum Chloride
  • Aluminum Compounds / toxicity*
  • Amphetamine / pharmacology
  • Animals
  • Animals, Newborn
  • Biomarkers
  • Cell Survival / drug effects
  • Cells, Cultured
  • Cerebral Cortex / drug effects*
  • Chlorides / toxicity*
  • L-Lactate Dehydrogenase
  • Neurons / cytology
  • Neurons / drug effects*
  • Neurotoxins / toxicity*
  • Pargyline / pharmacology
  • Rats
  • Rats, Wistar
  • Selegiline / pharmacology*

Substances

  • Aluminum Compounds
  • Biomarkers
  • Chlorides
  • Neurotoxins
  • Selegiline
  • Aluminum Chloride
  • Pargyline
  • Amphetamine
  • L-Lactate Dehydrogenase