Increased chloride transport in erythrocytes in Huntington's disease

W. A. Bialas, W. R. Markesbery, D. A. Butterfield

Research output: Contribution to journalArticlepeer-review

14 Scopus citations


Studies of 36Cl efflux across erythrocyte membranes in controls and Huntington's disease have been performed. An increased rate constant for 36Cl efflux in fresh Huntington's disease erythrocytes compared to normal controls was observed (P<0.01) in blind studies. Chloride transport is regulated in human erythrocytes at the external aspect of Band 3, the major red cell transmembrane protein. The present results on tissue completely outside the central nervous system are consistent with our suggestion that Huntington's disease is associated with a generalized membrane defect located at the external cell surface [Butterfield et al (1980) Life Sciences 27, 609–615].

Original languageEnglish
Pages (from-to)1895-1900
Number of pages6
JournalTopics in Catalysis
Issue number4
StatePublished - 1980

Bibliographical note

Funding Information:
This work was supported in part by the National Institutes of Health (NS-13791-03 and N8-14221) and the Muscular Dystrophy Association of America.

ASJC Scopus subject areas

  • Catalysis
  • General Chemistry
  • Biochemistry
  • Biophysics
  • Molecular Biology


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