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Experimental Porphyric Neuropathy: A Preliminary Report

Published online by Cambridge University Press:  18 September 2015

Anders A.F. Sima*
Affiliation:
Department of Pathology, Division of Neuropathology, Toronto General Hospital and University of Toronto, Toronto, Ontario, Canada; and Departments of Pathology and Radiation Oncology, Kingston General Hospital and Queen’s University, Kingston, Ontario, Canada
James C. Kennedy*
Affiliation:
Department of Pathology, Division of Neuropathology, Toronto General Hospital and University of Toronto, Toronto, Ontario, Canada; and Departments of Pathology and Radiation Oncology, Kingston General Hospital and Queen’s University, Kingston, Ontario, Canada
Dennis Blakeslee*
Affiliation:
Department of Pathology, Division of Neuropathology, Toronto General Hospital and University of Toronto, Toronto, Ontario, Canada; and Departments of Pathology and Radiation Oncology, Kingston General Hospital and Queen’s University, Kingston, Ontario, Canada
David M. Robertson*
Affiliation:
Department of Pathology, Division of Neuropathology, Toronto General Hospital and University of Toronto, Toronto, Ontario, Canada; and Departments of Pathology and Radiation Oncology, Kingston General Hospital and Queen’s University, Kingston, Ontario, Canada
*
Department of Pathology, Division of Neuropathology, Banting Institute, 100 College Street, Toronto, Ontario, M5G 11.5, Canada
Department of Pathology, Division of Neuropathology, Banting Institute, 100 College Street, Toronto, Ontario, M5G 11.5, Canada
Department of Pathology, Division of Neuropathology, Banting Institute, 100 College Street, Toronto, Ontario, M5G 11.5, Canada
Department of Pathology, Division of Neuropathology, Banting Institute, 100 College Street, Toronto, Ontario, M5G 11.5, Canada
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An experimental model for the study of porphyric neuropathy is presented. Injection of either tetraphenylporphinesulfonate (TPPS), hematoporphyrin derivative (HpD), or delta-aminolevulinic acid (ALA) into mice resulted in markedly decreased motor nerve conduction velocity (MNCV). The MNCV returned to normal within one week following the injection of large doses of A LA, and within three weeks following the injection of close to lethal doses of HpD. hut there was no recovery of nerve function within 60 days following injection of substantially smaller doses of TPPS. Ultrastructural examination of motor nerves at various times following TPPS injection revealed the gradual development of structural abnormalities. Ultrastructional examination of the same nerves after a single dose of either A LA or Hp D failed to demonstrate any abnormalities.

The present observations call for precaution as to the use of TPPS as photosensitizer in human cancer treatment.

Type
Articles
Copyright
Copyright © Canadian Neurological Sciences Federation 1981

References

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