title: Reduction of free radical activity in amyloid deposits following liver transplantation for familial amyloidotic polyneuropathy.
abstract: OBJECTIVE
  Liver transplantation halt the progress of familial amyloidotic polyneuropathy (FAP). Oxidative stress has been implicated in amyloid toxicity and formation. The objective of this study was to establish whether markers for oxidant stress and antioxidant capacity change following liver transplantation in patients with FAP.
  
  
  METHODS
  Morphometric and biochemical study.
  
  
  METHODS
  Tertiary referral centre.
  
  
  METHODS
  Duodenal biopsy samples from 16 patients, taken before and after liver transplantation were used for morphometry. Serum samples from 14 patients, seven of whom had received transplants, were analysed regarding antioxidant capacity.
  
  
  METHODS
  Liver transplantation.
  
  
  METHODS
  Immunohistochemistry was used to stain for the lipid peroxidation product 4-hydroxynonenal (HNE), and Congo red staining was used for amyloid detection. Positive areas were quantified by point counting. Total antioxidant capacity (TAC) was measured with a colourimetric assay.
  
  
  RESULTS
  In tissue, a decrease of HNE was noted after liver transplantation, whereas no significant changes were detected for amyloid deposits. No difference between transplanted and not transplanted patients was noted for total antioxidant capacity measured in serum.
  
  
  CONCLUSIONS
  To our knowledge, this is the first description of a reduction of markers for free radical activity after cessation of amyloid formation. The findings implicate that amyloid formation in transthyretin (TTR) amyloidosis generates oxidative stress, whereas amyloid deposits as such are less toxic to sourrounding tissues.
authors.affiliation: Department of Medicine, Umeå University Hospital, Sweden.
authors.forename: N
authors.initials: N
authors.lastname: Nyhlin
authors.forename: I
authors.initials: I
authors.lastname: Anan
authors.forename: Salhy M
authors.initials: SM
authors.lastname: El
authors.forename: Y
authors.initials: Y
authors.lastname: Ando
authors.forename: O B
authors.initials: OB
authors.lastname: Suhr
mesh_terms: D000328:Adult; D000447:Aldehydes / Q000378:metabolism; D028227:Amyloid Neuropathies, Familial / Q000473:pathology* / Q000601:surgery; D000686:Amyloidosis / Q000473:pathology*; D001706:Biopsy; D004386:Duodenum / Q000473:pathology; D005260:Female; D005500:Follow-Up Studies; D005609:Free Radicals / Q000378:metabolism; D006801:Humans; D007413:Intestinal Mucosa / Q000473:pathology; D015227:Lipid Peroxidation / Q000502:physiology*; D016031:Liver Transplantation / Q000473:pathology*; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress / Q000502:physiology*
chemical_list: D000447:Aldehydes; D005609:Free Radicals; C027576:4-hydroxy-2-nonenal