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Methionine 35 sulphoxide reduces toxicity of Aβ in red blood cell

Cristiana Carelli-Alinovi1, Francesco Misiti2

  • 1School of Medicine, Biochemistry and Clinical Biochemistry Institute, Catholic University, Rome, Italy.

European Journal of Clinical Investigation
|February 9, 2017
PubMed
Abstract

Insights

Oxidized amyloid-beta (Ab-sulphoxide) is less toxic in red blood cells (RBCs) due to increased pentose phosphate pathway (PPP) flux, suggesting a protective role in Alzheimer's disease.

Area of Science:

  • Neuroscience
  • Biochemistry
  • Cell Biology

Background:

  • Amyloid-beta (Ab) oxidation at methionine 35 to Ab-sulphoxide alters Ab neurotoxicity.
  • In nucleated cells, reduced Ab-sulphoxide toxicity correlates with increased methionine sulphoxide reductase A (MsrA) activity and mRNA levels.

Purpose of the Study:

  • To investigate if red blood cells (RBCs), lacking MsrA, exhibit a similar antioxidant response to Ab-sulphoxide.
  • To determine the role of the pentose phosphate pathway (PPP) in mitigating Ab-sulphoxide toxicity in RBCs.

Main Methods:

  • Exposing RBCs to Ab-sulphoxide and native Ab.
  • Measuring PPP flux and methionine oxidation levels in proteins.

Main Results:

  • Ab-sulphoxide exposure in RBCs led to increased PPP flux.
  • This increase in PPP flux correlated with reduced methionine oxidation in total proteins.
  • Native Ab did not induce these effects.

Conclusions:

  • The redox state of methionine 35 is crucial in modulating Ab-mediated events.
  • The pentose phosphate pathway (PPP) plays a protective role in RBCs, potentially relevant for Alzheimer's disease patients.
Keywords:
Alzheimer's diseaseamyloid beta-peptide (1-42)caspase 3methionine 35oxidative stresspentose phosphate pathwayred blood cell

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