Methionine 35 sulphoxide reduces toxicity of Abeta in red blood cell

Cristiana Carelli Alinovi, Francesco Misiti

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

Background: The oxidation of methionine residue in position 35 of Ab to sulphoxide (Ab-sulphoxide) has the ability to deeply modify wild-type Ab 1–42 (Ab) neurotoxic action. Our previous studies suggest that in nucleated cells, lower toxicity of Ab-sulphoxide might result not from structural alteration, but from elevation of methionine sulphoxide reductase A (MsrA) activity and mRNA levels. Design: On this basis, we hypothesised that red blood cell (RBC), a cell devoid almost completely of MsrA activity, shares with nucleated cells an antioxidant system induced by methionine 35 sulphoxide, responsible for the lower toxicity of Ab-sulphoxide in RBC. (Results) Supporting this hypothesis, we found that the low toxicity of Ab-sulphoxide in RBC correlated with pentose phosphate pathway (PPP) flux increase, and this event was associated with a low level of methionine oxidation in total proteins. None of these effects were observed when cells were exposed to Ab native. Discussion: These results outline the importance of the redox state of methionine 35 in the modulation of Ab-mediated events and suggest an important protective role for PPP in RBC of patients affected by Alzheimer's disease.
Original languageEnglish
Pages (from-to)314-321
Number of pages8
JournalEuropean Journal of Clinical Investigation
Volume47
DOIs
Publication statusPublished - 2017

Keywords

  • Alzheimer Disease
  • Alzheimer's disease
  • Amyloid beta-Peptides
  • Antioxidants
  • Biochemistry
  • Caspase 3
  • Clinical Biochemistry
  • Erythrocytes
  • Glucose
  • Healthy Volunteers
  • Humans
  • Methionine
  • Methionine Sulfoxide Reductases
  • Oxidation-Reduction
  • Pentose Phosphate Pathway
  • amyloid beta-peptide (1–42)
  • caspase 3
  • methionine 35
  • oxidative stress
  • pentose phosphate pathway
  • red blood cell

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