Ferric Ions Inhibit the Amyloid Fibrillation of β-Lactoglobulin at High Temperature

Biomacromolecules. 2015 Jun 8;16(6):1794-801. doi: 10.1021/acs.biomac.5b00371. Epub 2015 May 27.

Abstract

The energetics of amyloid fibrillar aggregation of β-lactoglobulin (βLG) following incubation at high temperature and acid pH was studied by differential scanning calorimetry in the presence of Cu(2+) or Fe(3+) cations, and without any metal. Cu(2+) and metal-free protein solutions showed a distinct exothermic response that disappeared almost completely when the Fe(3+) molar concentration was ten times greater than the βLG concentration. Thioflavin T fluorescence studies in solution and atomic force microscopy analysis of the deposit left on flat mica substrates by heat-incubated βLG solutions correlated the absence of exothermic response of Fe(3+)-βLG solutions with a lack of fibril production. In contrast, abundant fibril deposits were observed for Cu(2+)-βLG solutions, with a rich polymorphism of multistrand fibrillar structures. Electron paramagnetic resonance revealed that Fe(3+) permanently binds to βLG in the aggregate state whereas Cu(2+) plays a catalytic role without binding to the protein. We propose that Fe(3+) inhibits fibril production after binding to a key region of the protein sequence, possibly interfering with the nucleation step of the fibrillation process and opening a nonfibrillar aggregation pathway. These findings suggest that transition metal ions can be utilized to effectively modulate protein self-assembly into a variety of structures with distinct morphologies at the nanoscale level.

MeSH terms

  • Amyloid / chemistry*
  • Amyloid / drug effects
  • Hot Temperature
  • Hydrogen-Ion Concentration
  • Iron / chemistry*
  • Iron / pharmacology
  • Lactoglobulins / chemistry*
  • Lactoglobulins / metabolism
  • Protein Binding

Substances

  • Amyloid
  • Lactoglobulins
  • Iron